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Exercise therapy: spine 

Exercise therapy: spine
Chapter:
Exercise therapy: spine
Author(s):

Mark Comerford

DOI:
10.1093/med/9780199674107.003.0063
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Introduction: movement control impairments

For many years, clinicians have been convinced that impairments of movement control play an important role in the development and recurrence of painful conditions of the neuromusculoskeletal system (Comerford and Mottram 2001a, 2012, 2014; Janda 1985, 1995; Richardson et al. 1999; Sahrmann 2002, 2011). There is an evolving understanding of the importance of movement control, dynamic and static joint stability, and the co-ordination of muscle synergies in the management of neuromusculoskeletal impairments (Comerford and Mottram 2001a, 2012, 2014; Hides et al. 1996; Hodges and Richardson 1996; Jull 1997, 1998; Lee 1996; Mottram 1997; Mottram and Comerford 1999; O’Sullivan 2000; Richardson and Jull 1995; Richardson et al. 1999, 2004; Sahrmann 2002, 2011). Recent research has demonstrated the need to consider how movement is co-ordinated and controlled in the treatment of low back pain (LBP) (Hides et al. 1996; Hodges and Richardson 1996; O’Sullivan et al. 1997a; Richardson et al. 2004), cervical pain, and headaches (Jull et al. 1999).

The correction of movement control impairments or uncontrolled movement (UCM) should be based on a sound clinical assessment and clinical reasoning. The approach in the clinic should include three points: the best skills from current therapies, the best information from science, and the best therapeutic relationship with a particular patient (Butler 1998). This chapter highlights an approach to managing symptoms, impairments and disability, or activity limitations through assessing movement control impairments (uncontrolled movement) in the spine.

Concepts of muscle function and movement control

It is useful to consider the classification of muscles in relation to function when considering movement control and dynamic stability. The concept of classifying muscles by function gained general acceptance with Rood’s concept of stabilizer and mobilizer muscles (Goff 1972). Rood’s concept of differentiating stabilizer and mobilizer muscles has been further developed by Janda (1985) and Sahrmann (1993, 2002, 2011). Stabilizer muscles are described as having the characteristics of being mono-articular or segmental, deep, working eccentrically to control movement, and having static holding capacities. Mobility muscles on the other hand are described as bi-articular or multi-segmental, superficial, working concentrically with the acceleration of movement, and producing power. No other clinically accepted classification system was described until Bergmark presented the concept of local and global muscle systems when describing mechanical modelling of the spinal system (Bergmark 1989). In the local system, all muscles have their origin or insertion at the vertebrae and this system is used to control the curvature of the spine and provide stiffness to maintain mechanical stability of the lumbar spine. In the global system, the muscles are more superficial and link the thorax and pelvis. These muscles produce large torque/force.

Based on these concepts a new model of functional classification has been proposed (Comerford 1997; Comerford and Mottram 2001a, 2012, 2014) (Table 63.1). This model provides a subgrouping of muscles according to three distinct functional roles—a local stability muscle role, a global stability muscle role, and a global mobility muscle role (Comerford and Mottram 2001a, 2012, 2014; Mottram and Comerford 1999). The characteristics and function of the local stabilizer, global stabilizer, and global mobilizer muscles are described in Table 63.2. Examples are illustrated in Table 63.3.

Table 63.1 Model of reclassification of muscle function (by combining the strengths of the two previous models)

Stabilizer

Mobilizer

Local

Global

Local stabilizer function

Global stabilizer function

Global mobilizer function

Table 63.2 The function and characteristics of the three different muscle functional roles

Local Stabilizer Role

Global Stabilizer Role

Global Mobilizer Role

Function & characteristics

  • ↑ Muscle stiffness to control segmental motion

  • Controls the neutral joint position

  • Contraction = no/min; length change therefore does not produce range of motion

  • Activity is often anticipatory to functional load or movement to provide protective muscle stiffness prior to motion stress (feed-forward recruitment)

  • Activity is independent of direction of movement

  • Continuous activity throughout movement

  • Proprioceptive input re: joint position, range, and rate of movement

Function & characteristics

  • Generates force to control range of motion

  • Contraction = eccentric length change; therefore control throughout range, especially inner range (‘muscle active’ = ‘joint passive’) and hyper-mobile outer range

  • Functional ability to: (i) shorten through the full inner range of joint motion; (ii) isometrically hold position; (iii) eccentrically control the return against gravity and control hyper-mobile outer range of joint motion if present

  • Low load deceleration of momentum (especially axial plane: rotation)

  • Non-continuous activity

  • Activity is direction- dependent

Function & characteristics

  • Generates torque to produce range of movement

  • Contraction = concentric length change; therefore concentric production of movement (rather than eccentric control)

  • Concentric acceleration of movement (especially sagittal plane: flexion/extension)

  • Shock absorption of load

  • Activity is direction- dependent (predominately in the sagittal plane)

  • Non-continuous activity

    (on:off phasic pattern)

Table 63.3 Examples of classification of muscle functional roles

Local Stabilizer Role

Global Stabilizer Role

Global Mobilizer Role

For example:

  • Transversus abdominis

  • Segmental lumbar multifidus

  • Psoas (posterior fascicles)

  • Diaphragm

  • Pubococcygeus

  • Deep sacral gluteus maximus

  • Longus colli (longitudinal)

  • Sub-occipital cuff

  • Clavicular fibres of upper trapezius

For example:

  • Oblique abdominals

  • Superficial multifidus

  • Spinalis

  • Deep gluteus maximus

  • Deep gluteus medius

  • Psoas (anterior fascicles)

  • Levator ani

  • Longus colli (oblique fibres)

  • Semi-spinalis cervicus

For example:

  • Rectus abdominis

  • Iliocostalis

  • Longissimus

  • Latissimus dorsi

  • Quadratus lumborum (lateral fibres)

  • Rectus femoris

  • Tensor fascia latae (+ anterior iliotibial band)

  • Hamstrings

  • Superficial gluteus maximus (+ posterior iliotibial band)

  • Piriformis

  • Levator scapulae

  • Scalenae

  • Sternocleidomastoid

Muscle characterization: categorization according to role

Although these three different functional roles for muscles now appear to be well accepted, it has not been possible to characterize every muscle in the locomotor system according to one single subgroup or another. Understanding a muscle’s primary role is not always simple. Some muscles can easily be categorized into a subgroup, having only one specific functional role; however, other muscles appear to be capable of performing more than one of these functional roles (Comerford and Mottram 2012, 2014) Some muscles clearly exhibit all the characteristics of one subgroup and minimal characteristics of the others. They appear to have a single, very specific role and therefore their primary role can be defined as a local stabilizer or global stabilizer or global mobilizer. These muscles are single-task specific muscles. However, some muscles exhibit characteristics of more than one subgroup which cannot be explained by poor research methodology or misinterpretation of transversus abdominis, vastus medialis obliquus) or a global stabilizer role (e.g. external obliquus abdominis) or a global mobilizer role (e.g. rectus abdominis, hamstrings, iliocostalis lumborum). In the presence of pathology and/or pain, very specific impairments develop which are associated with the recognized specific primary functional role. The specific impairments are highly predictable and almost always present if they are assessed for. Very research results. They appear to be less specific and seem to be able to participate in a variety of different functional muscle roles without demonstrating impairment or dysfunction. These muscles are multi-taskcapable muscles (Comerford and Mottram 2012).

Single-task specific muscles

These muscles have a specific task-orientated role associated with being characterized as having only a local stabilizer role (e.g. specific retraining or correction strategies have been advocated in the treatment of the recovery of these predictable impairments (Hodges and Richardson 1996, 1997, 1999; Jull 2000; O’Sullivan 2000). This very specific training or corrective intervention is usually non-functional and as such is designed to correct very specific elements of impairment and dysfunction (Comerford and Mottram 2012). This specific retraining or correction may or may not integrate into normal functional activity. There is no way at the moment to predict or clinically measure automatic integration into normal function. In many subjects, this integration may need to be facilitated.

Multi-task capable muscles

These muscles appear to have a multi-tasking function associated with being characterized as having the potential to perform more than one role. That is, there is good evidence to support both a local role and a global role, or the evidence may support the muscle having a contribution to both stability and mobility roles (e.g. gluteus maximus, infraspinatus, and pelvic floor). They appear to contribute to combinations of local stabilizer, global stabilizer, and global mobilizer roles when required in normal function. In the presence of pathology and/or pain, a variety of different impairments and dysfunctions may present. These impairments can be identified as being associated with either one or several of the multi-tasking roles and appear to be related to recruitment deficiencies in an individual’s integrated stability system (Comerford and Mottram 2012). Treatment and retraining has to address the particular impairment or dysfunction that presents, usually needs to be multi-factorial, and should emphasize integration into ‘normal’ function.

Muscle physiology, pain, and recruitment

All human muscles have both fast and slow motor units and the function of the muscle is dependent on the recruitment of the motor units (Table 63.4). Dynamic postural control and normal low load functional movement is primarily a function of low threshold slow motor unit (tonic) recruitment. Low load (not high load or overload) exercise tends to optimize slow motor unit recruitment training. High load activity or strength training (endurance or power overload training) is a function of both slow (tonic) and fast (phasic) motor unit recruitment.

Table 63.4 Key features of slow and fast motor unit recruitment

Function

Slow Motor Units (low threshold or

tonic recruitment)

Fast Motor Units (high threshold or

phasic recruitment)

Load threshold

Low

(easily activated)

High

(requires greater stimulus)

Recruitment

Primarily recruited at low% of maximum voluntary contraction (<25%)

Increasingly recruited at higher% of maximum voluntary contraction (>40%)

Speed of contraction

Slow

Fast

Contraction force

Low

High

Fatiguability

Fatigue-resistant

Fast-fatiguing

Role

Fine control of postural activity and non-fatiguing low load ‘normal’ functional movements

Rapid or accelerated movement and fatiguing high load activity

There is consistent evidence of altered recruitment in the presence of pain. Pain affects slow motor unit recruitment more significantly than fast motor unit recruitment. Pain does not appear to significantly limit an athlete’s ability to generate power and speed so long as they can mentally ‘put the pain aside’. Research (Hodges and Moseley 2003) indicates that in the pain-free state, the brain and the central nervous system (CNS) are able to utilize a variety of motor control strategies to perform functional tasks and maintain control of movement, equilibrium, and joint stability. However, in the pain state, the options available to the CNS appear to become limited.

Recent research on musculoskeletal pain has focused on motor control changes associated with the pain state. This research has provided important new information regarding chronic or recurrent musculoskeletal pain. A large number of independent research groups are all reporting a common finding in their studies. They have consistently observed and measured that in the presence of chronic or recurrent pain, subjects change the patterns or strategies of synergistic recruitment that are normally used to perform low load functional movements or postures. They demonstrate that these subjects employ strategies or patterns of muscle recruitment that are normally reserved for high load function (e.g. lifting, pushing, pulling, throwing, jumping, running), for normal postural control, and low threshold functional activities. These altered (or limited) motor control strategies present as consistent co-contraction patterns, usually with exaggerated recruitment of the multi-joint muscles over the deeper segmental muscles, or as uncontrolled movement with impairments of movement control strategies (Comerford and Mottram 2012).

These altered strategies or patterns have been described in the research and clinical literature as ‘substitution strategies’, ‘compensatory movements’, ‘muscle imbalance’ between inhibited/lengthened stabilizers and shortened/overactive mobilizers, ‘faulty movements’, ‘abnormal dominance of the mobilizer synergists’, ‘co-contraction rigidity’, and ‘control impairments’.

Concept of restrictions and compensations to maintain functional movements

Movement control impairments may present as a disorder of articular translational movements at a single motion segment, e.g. abnormal articular translational motion. They may also present as a myofascial disorder in the functional movements across one or more motion segments, e.g. abnormal myofascial length and recruitment or as a response to neural mechanosensitivity. These two components of the movement system are inter-related and consequently articular translational and myofascial impairments often occur concurrently.

The inability to dynamically control movement at a joint segment or region may present as uncontrolled movement (UCM) or as an impairment of movement control. UCM is defined as a lack of active (or cognitive) low-threshold control of the local or global muscle’s ability to control motion at a particular site (joint or region of the body) in a particular direction or specific plane of motion (Comerford and Mottram 2012, 2014). UCM can present as a lack of control of normal functional motion or hypermobile range. It may be identified in the physiological or functional movements of joint range, or in the accessory translational gliding movements of a joint (Table 63.5). UCM is commonly (but not always) associated with a loss of motion or ‘restriction’ (Comerford and Mottram 2012, 2014).

Table 63.5 Key elements of restriction and uncontrolled compensation

Restriction

Compensation

(uncontrolled movement)

Articular restriction

  • Intra-articular and inter-articular joint hypomobility

Uncontrolled translation

  • Uncontrolled intra-articular and inter-articular joint hypermobility

Myofascial restriction

  • Lack of myofascial extensibility restricting range of motion

Uncontrolled range

  • Myofascial inability to control range of motion

The restriction may be associated with limitation of articular translation and a lack of extensibility of the connective tissue (intra-articular or peri-articular) at a motion segment. This presents with a loss of translational motion at a joint and is confirmed with manual palpation (e.g. Maitland et al. 2005). The restriction may be associated with a lack of extensibility of contractile myofascial tissue or neural tissue. The muscles may lose extensibility because of:

  1. i) increased low threshold recruitment or ‘over activity’ (Janda 1985; Sahrmann 2002, 2011)

  2. ii) a lack of range because of length-associated changes (Goldspink and Williams 1992; Gossman et al. 1982)

  3. iii) a lack of normal neural compliance and a protective response associated with abnormal neural mechanosensitivity (Balster and Jull 1997; Edgar et al. 1994; Hall and Elvey 1999; Hall et al. 1998).

These restrictions are confirmed with myofascial extensibility tests.

Movement control impairments can result in abnormal movement about several motion segments. When a muscle contracts it generates tension across motion segments at both ends, and if there is inadequate stability or control at any segment, then inappropriate motion may develop at this site. There is frequently, but not always, a restriction of normal motion (loss of physiological or accessory movement) at one or more motion segments, which contributes to compensatory excessive movement at adjacent segments in order to maintain function.

UCM often results from uncontrolled compensation for restriction. These movement control impairments may present as uncontrolled translation or uncontrolled range. When the UCM presents as uncontrolled translation, it is associated with laxity of articular connective tissue. Panjabi (1992) defined spinal instability in terms of laxity around the neutral position of a spinal segment called the neutral zone. Maitland et al. (2005) have described joint hypermobility. The end result of this process is abnormal development of uncontrolled movement and a loss of functional or dynamic stability. Articular translational UCM can compensate for:

  1. i) articular restriction in the same joint (restriction and compensation at an intra-articular level),

  2. ii) articular restriction in an adjacent joint (restriction and compensation at an inter-articular level),

  3. iii) myofascial restriction (restriction and compensation at a regional level).

When the UCM presents as uncontrolled range, it is associated with excessive length or poor control of myofascial tissue. This is the usual compensation for:

  1. i) myofascial restriction at an adjacent region (restriction and compensation at a regional level),

  2. ii) abnormal mechanosensitivity at an adjacent region (restriction and compensation at a regional level),

  3. iii) segmental articular translational restriction at an adjacent joint (restriction and compensation at an inter-articular level).

Uncontrolled translation and uncontrolled range can present in isolation without restriction. Common examples of this type of presentation are:

  1. i) a traumatic incident (capsular/ligamentous laxity or instability),

  2. ii) inhibition associated with pain and pathology,

  3. iii) sustained postural strain positioning.

The UCM may be due to muscle inhibition associated with abnormal neural mechanosensitivity.

In the functional movement system, the site of UCM is the site of the movement control impairment (Comerford and Mottram 2012, 2014). The uncontrolled segment or region is the most likely source of pathology and symptoms of mechanical origin. The direction of UCM relates to the direction of tissue stress or strain and pain-producing movements (Comerford and Mottram 2012; Sahrmann 2002, 2011). It is important, in the assessment of movement control impairments, to identify the region and the direction of UCM and relate it to the symptoms and pathology.

The clinical testing for movement control impairments identifies the segment and the direction of uncontrolled movement that are related to the direction of symptom- producing movement. The identification of UCM into excessive uncontrolled lumbar flexion, under flexion load, may place abnormal stress or strain on various tissues and result in flexion-related symptoms. Likewise, the identification of UCM into uncontrolled lumbar extension, under extension load, produces extension-related symptoms; while uncontrolled lumbo-pelvic rotation or side-bend/side-shift, under unilateral load, may produce unilateral symptoms. Stiff or restricted segments are not usually the source of pain during normal functional movement or loading, although pain may be elicited under abnormal movement or load. Generally, the stiff or restricted segment may be a cause of compensatory UCM at an adjacent joint.

Restriction Compensation Uncontrolled Movement  (UCM) Pathology Pain

Although it is commonly observed that restrictions are compensated for by increasing movement elsewhere in the body, it is incorrect to assume that all compensation is uncontrolled. A compensation that demonstrates efficient active or cognitive control during testing for movement control impairments is a normal compensation strategy and does not constitute UCM and usually does not contribute to symptoms. However, compensation that fails to demonstrate this is an aberrant compensation strategy (Comerford and Mottram 2012, 2014).

It is important to relate the site and direction of UCM to symptoms and pathology and to the mechanisms of provocation of symptoms. Management of the movement control impairment that relates to the symptoms and pathology becomes the clinical priority. UCMs that may be evident, but do not relate to symptoms, are not a priority of pathology management. However, it may indicate a potential risk for the future. The movement control impairment can be labelled (or diagnosed) by the side and direction of UCM. Common patterns seen in the clinic are described in Tables 63.6 and 63.7.

Table 63.6 Lumbar spine movement control impairments

Lumbar spine

movement control impairment

Direction of UCM

(uncontrolled compensation)

Common symptom presentation

Lumbar flexion UCM

Lumbar flexion under flexion load

Pain in lumbar spine (+/− referred)—aggravated or provoked by flexion load, movements, or flexed postures

Lumbar flexion rotation UCM

Lumbar rotation and flexion under unilateral load

Unilateral pain in lumbar spine (+/− referred)—aggravated or provoked by unilateral load or flexion load, movements, or flexed postures

Lumbar extension UCM

Lumbar extension under extension load

Pain in lumbar spine (+/− referred)—aggravated or provoked by extension load, movements, or extended postures

Lumbar extension rotation UCM

Lumbar rotation and extension under unilateral load

Unilateral pain in lumbar spine (+/− referred)—aggravated or provoked by unilateral load or extension load, movements, or extended postures

Lumbar global (multi-directional) UCM

Lumbar flexion and extension and rotation under related load tests

Pain in lumbar spine (central or unilateral) (+/− referred); flexion symptoms provoked by flexion load or movements (especially prolonged sitting); extension symptoms provoked by extension load or movements (especially prolonged standing); unilateral symptoms provoked by unilateral load or movements (especially static asymmetrical postures)

Table 63.7 Cervical spine movement control impairments

Cervical spine

movement control impairments

Direction of UCM

(uncontrolled compensation)

Common symptom presentation

Upper cervical extension UCM

Upper cervical extension under extension load

Upper cervical pain (+/–headaches or referral)—aggravated or provoked by extension load, movements, or postures

+/− rotation/sidebend

Cervical extension or lateral flexion during rotation

Unilateral pain in upper cervical spine—aggravated or provoked by unilateral load or movements

Low cervical flexion UCM

Low cervical flexion under flexion load

Low cervical pain (+/− referred)—aggravated or provoked by flexion load, movements, or postures

+/− rotation/sidebend

Cervical lateral flexion during rotation

Unilateral pain in upper cervical spine—aggravated or provoked by unilateral load or movements

Mid cervical translation UCM

Mid cervical (usually translational shear C3-4 or C4-5) under extension load

Mid cervical pain (+/–referred)—aggravated or provoked by extension load, movements, or postures

+/− rotation/sidebend

Cervical extension or lateral flexion during rotation

Unilateral pain in upper cervical spine—aggravated or provoked by unilateral load or movements

Upper cervical flexion UCM

Upper cervical flexion under flexion load

Upper cervical pain (+/− headaches or referral)—aggravated or provoked by flexion load, movements, or postures (often traumatic involving upper cervical ligamentous laxity, e.g. forced flexion injury)

+/− rotation/sidebend

Upper lateral flexion during rotation

Unilateral pain in upper cervical spine—aggravated or provoked by unilateral load or movements

Evidence of movement control impairment

Movement control impairments can be identified in the local and global muscle systems (Table 63.8). They can occur as aberrant recruitment and motor control of the deep local muscle stability system, resulting in poor control of the neutral joint position (Hides et al. 1996; Hodges and Richardson 1996; Jull et al. 1999; O’Sullivan et al. 1997b; Richardson et al. 1999, 2004). This literature demonstrates a motor control deficit associated with delayed timing or inefficient low threshold recruitment in the local stability system. These changes may decrease the efficiency of muscle action around a motion segment and potentially result in poor segmental control and instability (Cholewicki and McGill 1996).

Table 63.8 Recruitment impairment in the three muscle functional roles

Local Stabilizer Role

Global Stabilizer Role

Global Mobilizer Role

Impairment:

  • ↑ Motor control deficit associated with delayed timing or recruitment deficiency

  • Reacts to pain and pathology with inhibition

  • ↑ Muscle stiffness and poor segmental control

  • Loss of control of joint neutral position

Impairment:

  • Muscle lacks the ability to (i) shorten through the full inner range of joint motion; (ii) isometrically hold position; (iii) eccentrically control the return

  • Muscle active shortening = joint passive (loss of inner range control)

  • If hyper-mobile—poor control of excessive range

  • Poor low threshold tonic recruitment

  • Poor eccentric control

  • Poor rotation dissociation

Impairment:

  • Loss of myofascial extensibility—limits physiological and/or accessory motion (which must be compensated for elsewhere)

  • Over-active low threshold, low load recruitment

  • Reacts to pain and pathology with spasm

Result:

Local inhibition

Global imbalance Exercise therapy: spine

(inefficient, centrally down-regulated global stabilizer)

Global imbalance

(overactive/short, centrally up-regulated global mobilizer)

Hodges and Richardson (1996) investigated the contribution of the transversus abdominis to spinal stabilization in subjects with and without LBP. The delayed onset of contraction of the transversus abdominis in subjects with LBP indicates a deficit of motor control and, as a result of this, the authors hypothesize that there would be inefficient muscular stabilization of the spine. From the evidence to date, it would appear that in all back pain subjects, the transversus abdominis has a recruitment impairment that is independent of the type or nature of pathology, while subjects who have never had significant back pain do not have this impairment (Hodges and Richardson 1996; Richardson et al. 2004). The recruitment impairment is related to motor control deficits, not strength.

There is evidence of lumbar multifidus muscle reduction in a cross-sectional area ipsilateral to symptoms in patients with acute/subacute LBP (Hides et al. 1994). This decrease in size of the multifidus was seen on the side of the symptoms with the reduced cross-sectional area observed at a single vertebral level, suggesting segmental pain inhibition. This evidence suggests that pain and impairment are related (Stokes and Young 1984). In acute onset back pain, this immediate inhibition of the lumbar multifidus does not automatically return when symptoms settle. It has been observed that recovery of symmetry was more rapid and more complete in patients who received specific, cognitive, localized multifidus and transversus abdominis muscle recruitment retraining (Hides et al. 1996).

Dangaria and Naesh (1998) assessed the cross-sectional area of the psoas major in unilateral sciatica caused by disc herniation. There was significant reduction in the cross-sectional area of the psoas at the level and site of disc herniation on the ipsilateral side. Segmental inhibition due to pathology and pain may be responsible for the psoas reduction in the cross-sectional area.

Inhibition of the local stability system has also been demonstrated in subjects with headaches (Jull et al. 1999). Deep neck flexor muscle contraction was significantly inferior in the cervical headache group.

There is a common model of stability in the lumbar spine relating it to a cylinder. Richardson et al. (1999, 2004) use a cylinder concept to describe the local stability system for the lumbo-pelvic region. They suggest the transversus abdominis and the spinal column make up the wall of the cylinder, with the diaphragm and pelvic floor muscles making up the top and bottom respectively. In the light of recent research, perhaps the stability cylinder model can be updated (Figure 63.1). Consider the spine as a flexible segmented structure embedded in the wall of the cylinder. The role of the cylinder is to support and stabilize this flexible structure while it moves. The cylinder can be portrayed as having an inner (local) core and an outer (global) shell (Comerford and Mottram 2012). The wall of the inner local core of the cylinder is made up of the transversus abdominis providing lateral control and resistance to segmental displacement laterally. The spine is stabilized posteriorly by segmental attachments of the lumbar multifidus and stabilized anteriorly by segmental attachments of the psoas (posterior fascicles). These two muscles provide sagittal and axial control and resistance to antero-posterior and rotatory segmental displacement. Their longitudinal fibre placement contributes to axial compression to enhance stability throughout the spinal range of motion. Tension generated by these muscles also contributes to increasing fascial tension to improve the load-bearing ability of the spine.

Figure 63.1 Functional stability cylinder for the trunk

Figure 63.1
Functional stability cylinder for the trunk

(reprinted with permission from Movement Performance Solutions).

The cylinder requires a top and bottom if it is to increase internal pressure, known as intra-abdominal pressure (IAP), to enhance spinal stability. If IAP is to assist in spinal stabilization, it must be able to generate pressure independently from respiratory and continence functions. It has been demonstrated that the costal part of the diaphragm has a stability role independent from respiration, although it also contributes to respiratory function (Hodges and Gandevia 2000). It is theorized that the pubo-visceral muscles (e.g. pubococcygeus) have the stability role within the pelvic floor (Sapsford et al. 1997).

If the model of a local core is valid, then these muscles must have efficient recruitment and have sophisticated co-ordination and integration processes. It seems logical that if any one of these muscles is dysfunctional, then the stability of the cylinder will be compromised unless the other muscles (or some other process) can adequately compensate.

The outer global shell of the cylinder consists of the global stabilizer muscles and the global mobilizer muscles acting around the trunk (Comerford and Mottram 2012). The global stabilizer muscles, such as the oblique abdominals, anterior fasiculus of psoas, superficial multifidus, and spinalis, act to eccentrically control range of motion and decelerate rotational forces across the trunk. The global mobilizer muscles, such as the rectus abdominis, iliocostalis, longissimus, and quadratus lumborum, act to produce fast, large-range, and forceful movement. When the integrated local cylinder function can be achieved, then the local core and the global shell should be retrained to ensure co-ordinated normal function. The global stability of the trunk is essential for proximal control of the spine and girdles during limb motion and functional loading. If the local cylinder has re-established normal efficient function, then under low load normal functional demands, it should recruit automatically whenever the global system is required to work.

Movement control impairments can occur globally as imbalance between the mono-articular stabilizers and the bi-articular mobilizers or movement-producing muscles (Rood, as reported by Goff 1972; Janda 1985; Kankaanpaa et al. 1998; Sahrmann 1993, 2002). This imbalance presents in terms of alteration in functional length tests and recruitment patterns of these muscles.

Clinically, it can be seen that the global stability muscles lack the ability to shorten through the full range of joint motion. They also demonstrate poor low load or low threshold recruitment (Janda 1995; Sahrmann 2002, 2011) and poor low load eccentric control of rotation (Comerford and Mottram 2002a,b,c,d; Sahrmann 2002, 2011). For example, gluteal dysfunction has been associated with lumbo-pelvic pain (Janda 1985; Kankaanpaa et al. 1998). With over-activity in the global mobility muscles, clinical examination demonstrates myofascial shortening which limits motion (Sahrmann 2002, 2011). For example, the over-activity of the rectus abdominis, rectus femoris, tensor fascia latae, and the hamstrings can have a significant influence on the compensatory movement of the pelvis and lumbar spine. A similar influence can be observed in the cervical spine with over-activity and/or shortness of, for example, the levator scapulae and scalanae.

Recruitment impairment in the global muscle system may result in abnormal centrally mediated up-regulation and ‘over-activity’ of muscles with a global mobilizer role, along with concurrent centrally mediated down-regulation and inefficiency of muscles with a global stabilizer role. This ‘imbalance’ in the control and co-ordination of recruitment between joint stabilizer muscles and their joint mobilizer synergists results in altered forces acting around a motion segment. The loss of ideal or normal local or global control may result in abnormal stress or strain being imposed on the joint, its supporting soft tissue structures, and related myofascial tissue and neural tissue. As a result of these movement control impairments, tissue stress and microtrauma may exceed the tissues’ tolerance and ability to recover, with pathology and pain developing over time.

The assessment for movement control impairments must identify changes in the recruitment of muscles in the local stability system and recruitment, length, and force efficiency changes in the global stability system (Comerford and Mottram 2012).

Clinical examination for movement control impairment

The clinical examination aims to identify movement control impairments and relate these impairments to pain in the movement system. The movement system is made up of articular, myofascial, neural, and connective tissue systems of the body. Good function requires the integrated and co-ordinated interaction of these systems. Each system needs to be examined and the influence of one system on the other needs to be considered. For example, pain, pathology, disuse, and abnormal proprioceptive input can inhibit muscle recruitment (Brumagne et al. 1999; Hurley and Newham 1993; Stokes and Young 1984; Taimela et al. 1999). This inhibition can be noted in muscles with a local stability role and a global stability role. Noxious input, for example pain, may produce muscle ‘spasm’ (Schaible and Grubb 1993). Clinically, this ‘spasm’ is primarily observed in the global mobility muscles. This is seen as a typical pattern in patients with LBP, i.e. over-activity and centrally mediated up-regulation in the large superficial erector spinae, while at the same time, inhibition is observed in the segmental fibres of the lumbar multifidus.

Proprioception can influence muscle function at peripheral joints (Hurley 1997) and may have an influence on spinal muscle function (Brumagne et al. 1999; Taimela et al. 1999). Pain, pathology, sensitized neural tissue, and altered proprioceptive input can all influence recruitment of muscles that perform a local or global stability role, thus affecting functional stability and movement control. Therefore, it is important to assess function and impairment in all components of the movement system.

Sahrmann (1993, 2002, 2011) emphasizes the importance of considering the factor of cumulative microtrauma as a cause of musculoskeletal pain and states, ‘faulty movement can induce pathology, not just be a result of it’. This cumulative microtrauma can result from repetitive activities or from complex changes in patterns of multi-joint movements. For this reason, movement patterns need to be examined in detail, and a history of activities and functional activities analysed. In view of the changes in muscle function in the local and global systems, the physical examination must include an assessment of muscle function: local stability muscles, global stability muscles, and global mobility muscles. Specific tests need to be considered (Table 63.9).

Table 63.9 Differentiation between low threshold recruitment impairment and high threshold strength/speed performance

Movement and performance dysfunction

Low threshold movement control impairments

High threshold strength/ speed impairments

Assessment

Identified by the failure to control movement under non-fatiguing low-load testing

Identified by the failure to perform movement under fatiguing high-load testing

Result

Results in the development of uncontrolled movement, pathology, and pain

Results in weakness and loss of performance

The diagnosis of uncontrolled movement (UCM): direction control

In pain-free function, all muscles work and co-activate in integrated patterns to produce and control movement during all normal functional activities. All functional activities impose stress and strain forces on the movement system in varying loads and in all three planes or directions of motion, and normal functional movements rarely eliminate motion from one joint system while others move through range. Functional movement rarely occurs in only one plane.

However, everybody has the ability to perform patterns of movement that are not habitually used in ‘normal function’ (e.g. pat the head and rub the stomach). Performance of some of these unfamiliar movements is a test of motor control (skill and co-ordination). The ability to activate muscles to isometrically hold position or to control/prevent motion at one joint system, while concurrently actively producing a movement at another joint system in a specific direction, is a test of movement control efficiency (Comerford and Mottram 2012).

The process of dissociating movement at one joint from movement at another joint has potential benefits for retraining the stability muscles to enhance their recruitment efficiency to control direction-specific stress and strain. The global and the local stability muscle systems can be trained to recruit in co-activation patterns to prevent movement in a specific direction at a vulnerable, painful, or unstable joint, while an adjacent joint is loaded in that direction. In this way, the movement control system can be trained to control a specific site and direction of UCM (Comerford and Mottram 2012).

The global muscles react to pain and pathology with functional length and recruitment impairments. The assessment of global muscle function considers the ability to dissociate direction and control of through-range motion. The global stability muscles are required to control directional strain, i.e. cognitively or actively control the excessive UCM into flexion/extension or rotation to certain benchmark standards. The assessment for the ability of the global stability muscles to control direction- related stress and strain involves actively controlling and preventing movements of the spine into flexion, extension, rotation, or sidebending, while moving the limbs independently into flexion, extension, rotation, and other directions. These movement control tests are not natural or ‘normal’ functional movements, but rather, are movement patterns that everybody should have the ability to perform given the instruction to do so and a short period of teaching and familiarization (Comerford and Mottram 2012; Hamilton 1998; Sahrmann 2002, 2011). Some examples of movement control tests that are used to identify the site and direction of UCM are highlighted here.

In the cervical spine, a symmetrical range of cervical rotation should be achieved. Symmetry is important but range is variable. The common directions of UCM are upper cervical—extension UCM (chin poke associated with poor recruitment efficiency of the deep neck flexor stabilizer muscles) and cervical—lateral flexion UCM during rotation (associated with a coupling dysfunction in the articular system and/or poor recruitment efficiency of the deep neck flexors) (Figure 63.2). A significant asymmetry of rotation or an obvious decrease in range of motion is seen when the UCM is actively or passively controlled. Restriction may occur from articular translational dysfunction or myofascial dysfunction or related neural sensitivity.

Figure 63.2 Cervical rotation control

Figure 63.2
Cervical rotation control

(reprinted with permission from Physiotools).

Two useful tests for lumbar flexion UCM are the standing forward lean test and the sitting forward lean test.

  • Standing forward lean test (Comerford and Mottram 2012; Sahrmann 2002) (Figure 63.3): the subject is instructed to stand tall and to bend or ‘bow’ forwards from the hips, keeping the back straight (neutral spine), and prevent or control any lumbar flexion or posterior tilt increasing at the lumbar pelvic area. Ideally, the subject should have the ability to dissociate the lumbar spine from hip flexion as evidenced by 50° forwards lean while preventing or controlling lumbar flexion and maintaining the lumbar spine neutral position. A positive test for lumbar flexion UCM will demonstrate a lack of ability to control or prevent lumbar flexion throughout the benchmark range of direction control to 50° forwards leaning.

  • Sitting forward lean test (Comerford and Mottram 2012; Hamilton 1998; Sahrmann 2002) (Figure 63.4): the subject is instructed to sit tall and to lean forwards from the hips, keeping the back straight (neutral spine). Ideally, the subject should have the ability to dissociate the lumbar spine from hip flexion as evidenced by 30° of forwards lean with maintenance of the lumbar spine neutral position. A positive test for lumbar flexion UCM will demonstrate an inability to control or prevent lumbo-sacral flexion and posterior tilt occurring before the benchmark of 30° forwards leaning. A positive test for lumbar extension UCM will demonstrate an inability to control or prevent lumbar extension and anterior tilt occurring before the benchmark of 30° forwards leaning.

Figure 63.3 Lumbar flexion control—standing forward lean

Figure 63.3
Lumbar flexion control—standing forward lean

(reprinted with permission from Physiotools).

Figure 63.4 Lumbar flexion control—sitting forward lean

Figure 63.4
Lumbar flexion control—sitting forward lean

(reprinted with permission from Physiotools).

Supine bent knee fallout (Comerford and Mottram 2012; Sahrmann 2002) is a useful test to identify a lumbo-pelvic rotation UCM (Figure 63.5). With the subject lying supine and with legs extended and the feet together, both anterior superior iliac spines (ASISs) are checked for symmetry in the antero-posterior plane. The subject is instructed to slide one heel up beside the other knee. Ideally, the pelvis should not rotate and the ASIS remains level. If the pelvis stays stable and does not rotate, the subject is instructed to slowly lower the bent leg out to the side, keeping the foot supported beside the straight leg. There is usually some slight rotation of the pelvis at this stage. The subject is then instructed to repeat the ‘bent leg fallout’ but not to allow the pelvis to rotate at all. Ideally, the bent leg should be able to be lowered through the available range of hip abduction and lateral rotation (at least 50°) and returned, without associated pelvic rotation. A positive test for lumbo-pelvic rotation UCM will demonstrate an inability to control or prevent pelvic rotation occurring before the benchmark of 50° leg abduction and lateral rotation out to the side.

Figure 63.5 Lumbar rotation control—bent knee fallout

Figure 63.5
Lumbar rotation control—bent knee fallout

(reprinted with permission from Physiotools).

Local stability muscle role: control of intersegmental displacement in neutral joint position

In the presence of regional pathology or pain, the local stability muscles demonstrate recruitment impairments, and specific tests have been designed to assess these impairments (Hides et al. 1996; Hodges and Richardson 1996; Jull 1998; Jull et al. 1999; Richardson and Jull 1995; Richardson et al. 1999, 2004). These tests must identify and exclude substitution strategies from the global muscles, e.g. during a low abdominal hollowing recruitment strategy for the transversus abdominis, observe and palpate for excessive activity of the external obliques and rectus abdominis.

To test for the stability function of the deep neck flexors (longus colli), the subject is positioned in supine position with the spine, temporomandibular joint (TMJ), and scapula in a neutral position (head supported on towel). The subject is instructed to perform a very slight upper cervical flexion action (cranio-cervical flexion), which causes a slight cervical flexion and flattening of the cervical curve. A pressure biofeedback unit (‘Stabilizer’, manufactured by the Chattanooga Group, Australia) can be used to measure function (Jull 1998, 2000, 2001) (Figure 63.6). There should be no substitution (for example, from the scalenae or sternocleidomastoid) or fatigue. A flattening pressure (6–8 mmHg in 2-mmHg increments) should be sustained for 10 seconds with 10 repetitions (Jull 1998). There should be minimal range of movement.

Figure 63.6 Deep neck flexor control of neutral position

Figure 63.6
Deep neck flexor control of neutral position

(reprinted with permission from Physiotools).

The transversus abdominis will tension the low abdominal fascia and hollow the low abdominal wall. This ‘drawing in’ or ‘low abdominal hollowing’ action should be specifically localized to the lower abdominal region and there should be minimal spinal or pelvic tilt or rib cage movement. It should not cause lateral flaring of the waist. A pressure biofeedback unit (‘Stabilizer’, manufactured by the Chattanooga Group, Australia) can be used to measure a function of transversus abdominis recruitment in prone lying (Figure 63.7) (Cairns et al. 2000; Hodges et al. 1996; Richardson et al. 1999, 2004). For good motor control patterns, the patient needs to be able to specifically activate a dominant transversus contraction using the lower abdominal hollowing strategy, and maintain this contraction consistently during relaxed breathing. The activation strategy should be repeated several times in a variety of different functional postures such as lying, supported sitting, and supported standing. A useful guide is a 10-second hold with 10 repetitions (Richardson and Jull 1995; Richardson et al. 2004).

Figure 63.7 Transversus abdominus activation in neutral position

Figure 63.7
Transversus abdominus activation in neutral position

(reprinted with permission from Physiotools).

To test for lumbar multifidus function, the multifidus is consciously activated against the facilitating pressure of a thumb/finger (Hides et al. 1996; Richardson et al. 1999) (Figure 63.8). This contraction ideally should be maintained for 10 seconds and consistently repeated 10 times. Substitution strategies, for example, excessive substitution of the erector spinae or lumbar extension/pelvic tilt, should be avoided.

Figure 63.8 Lumbar bifidus activation in neutral position

Figure 63.8
Lumbar bifidus activation in neutral position

(reprinted with permission from Physiotools).

To test for recruitment of a local stability role for the psoas major (posted fascicles), the patient lies on one side with both legs bent. The top femur is supported horizontally with the spine, pelvis, and upper trunk all in neutral alignment. The local stabilizer role of the psoas major is evaluated with a longitudinal activation strategy. The psoas is facilitated by gently distracting the top leg longitudinally and the patient is instructed to ‘gently pull the hip back into the socket’ without moving the spine or pelvis (Comerford and Mottram 2014). Facilitation may be localized segmentally. The therapist manually palpates the relative stiffness at that level, attempting to translate the spinous process side to side. The psoas activation is facilitated and resistance to manual translation (stiffness) is re-assessed (Comerford and Emerson 1999). Ideally, a significant increase in resistance to manual displacement should be noted when the psoas is activated. The contraction (and increased stiffness) should be maintained for 10 seconds and consistently repeated 10 times. This response should be noted at all lumbar segmental levels.

Segmental psoas recruitment impairment is identified by identifying the level that does not increase resistance to manual translation when compared to adjacent levels (which do increase resistance to translation when the psoas is activated with the longitudinal activation strategy). A lack of increased resistance to manual displacement during psoas activation indicates a probable loss of segmental control of the local stability role of the psoas (Comerford and Mottram 2014).

Global muscle imbalance—recruitment synergies: global stabilizer down-regulation

In normal pain-free function, the one-joint global stability muscles are designed to have the ability to move body segments against gravity through the full available range of joint motion. The global stabilizers are normally dominant to their multi-joint global mobilizer synergists during non-fatiguing submaximal normal function. The global mobilizer synergists are designed to be dominant to the global stabilizers for high load fatiguing function. When global stability muscles demonstrate recruitment impairment, for example during episodes of musculoskeletal pain, they present with centrally mediated down-regulation or inhibition. They respond less efficiently to non-fatiguing loads and low threshold stimuli and demonstrate an inability to move the body segments throughout the full inner range of joint motion. For example, through range control of the cervico-thoracic stabilizing extensors (semi-spinalis) is required to control segmental cervico-thoracic extension and eccentric cervico-thoracic flexion. Clinically, it is frequently observed that the gluteus maximus loses the ability to control hip extension to the inner range. The global stability muscles must have the ability to move the joint through the full available range in normal non-fatiguing function. These examples are illustrated here.

  • Semi-spinalis inner-range control (Comerford and Mottram 2014)—through-range control of the cervico-thoracic stabilizing extensors (Figure 63.9): The subject starts by resting prone on elbows, with the scapulae and thoracic spine neutral and the head hanging in flexion. The subject is instructed to maintain the upper cervical spine in flexion or neutral and lift their head with independent extension of the low cervical spine through the full range and lower the head to return to the starting position. Ideally, the subject should have the ability to independently extend the lower cervical spine through the full range of extension and hold in the shortened range position for 10 seconds without fatigue or substitution; then return, with eccentric control, to the starting position in the outer range without substitution. Activation of the mobility muscles under load is normal. When the movement is performed correctly (without substitution or fatigue), the range that can be controlled actively equals the available passive range of cervical flexion.

  • Gluteus maximus inner-range control (Comerford and Mottram 2014)—hip extension with knee flexed, prone position (Figure 63.10): With the subject lying prone and one knee flexed to past 90°, the lumbo-pelvic region is manually stabilized and the hip passively lifted into extension to check the available range of hip extension. The subject is instructed to lift the knee (hip extension) approximately 3 to 5 cm (1 to 2 inches). Note any lack of gluteal participation, cramping of the hamstrings, or excessive lumbar extension or rotation under hip extension load. Ideally, the lumbo-pelvic region should maintain a neutral position as the hip actively extends (approximately 10–15°). Hip extension should be initiated and maintained by the gluteus maximus. The muscle should have the ability to shorten sufficiently and hold the limb load in the joint inner-range position for 10 seconds, and repeat the movement 10 times (without the inner-range hold) and without substitution or fatigue. The hamstrings will participate in the movement but should not dominate. There will be paraspinal muscle activation (asymmetrically biased) but there should be no gross hyperextension, segmental shear (pivot), or rotation in the lumbar spine.

Figure 63.9 Cervico-thoracic extensor stabilizers—through-range control

Figure 63.9
Cervico-thoracic extensor stabilizers—through-range control

(reprinted with permission from Physiotools).

Figure 63.10 Gluteus maximus—inner-range control

Figure 63.10
Gluteus maximus—inner-range control

(reprinted with permission from Physiotools).

Global muscle imbalance—recruitment synergies: global mobilizer up-regulation

In the presence of chronic or recurrent musculoskeletal pain, one-joint global stabilizer synergists become inhibited and less efficient. In this situation, the global mobilizer synergists appear to become up-regulated and demonstrate increased recruitment of slow motor units, ‘taking over’ from the global stabilizers to become the dominant synergists to perform postural control tasks and non-fatiguing functional movements. Over time, as the global mobilizers participate excessively with increased tonic, slow motor unit recruitment in postural control tasks, the global mobilizer muscles lose extensibility. This loss of extensibility usually requires that some other motion segment increases movement as a compensation to maintain function. When the global mobility muscles lose extensibility, there may be changes in the contractile or connective tissue elements of the muscle. Recruitment issues or mechanical issues may influence these elements. The global mobility muscles need to be examined for length and recruitment changes.

  • Assessment for hamstring extensibility (Comerford and Mottram 2014) (Figure 63.11): The subject sits with the spine and pelvis in neutral alignment, the acromion vertically positioned over the ischium, the hips flexed at 90° and the feet unsupported. The operator monitors the lumbo-pelvic position and passively extends the knee until either resistance to extension is felt (stretch in the posterior thigh) or there is a loss of lumbo-pelvic neutral position. Ideally, with maintenance of lumbo-pelvic neutral position and the hip flexed to 90°, the knee should be able to extend to within 10° of full extension. The lumbar spine should not flex and the pelvis should not posteriorly tilt or rotate. The shoulders should stay vertically aligned over the ischium and not lean back into hip extension.

  • Assessment for levator scapula extensibility (Comerford and Mottram 2014) (Figure 63.12): Position the subject with cervical spine and scapula in neutral position (lying). The cervical spine is flexed, the head rotated and laterally flexed away from the side to be assessed. The head is moved until the extensibility limit of the levator scapula is reached or the scapula elevates to follow the muscle. Maintain this position and take tension off the muscle by passively elevating the shoulder. Then attempt to move the head into more range of lateral flexion. If there is no further available range, the cervical spine is at the limit of motion and the levator scapula muscle is not short. If there is more range available, then the levator scapula is short and limiting function.

Figure 63.11 Hamstrings extensibility

Figure 63.11
Hamstrings extensibility

(reprinted with permission from Physiotools).

Figure 63.12 Levator scapulae extensibility

Figure 63.12
Levator scapulae extensibility

(reprinted with permission from Physiotools).

Rehabilitation strategies for regaining control of uncontrolled movement

The retraining of movement control impairments will depend on the pattern of the impairment and the site and direction of the UCM. From the assessment of articular translational and myofascial restriction and for uncontrolled translation and range, retraining priorities can be identified. Making a diagnosis of the site and direction of UCM using movement control impairment tests, and then using this diagnosis to begin direction control retraining is a good first step in managing mechanical musculoskeletal pain. Correcting movement control impairments and recruitment patterns is the priority in the rehabilitation of the local stability system. Correcting length and impairments in the patterns of synergist recruitment between global stabilizers and global mobilizers is the priority of the global system. Addressing the restriction on uncontrolled compensation is the key to rehabilitation (Table 63.10) (Comerford and Mottram 2001b, 2012).

Table 63.10 Rehabilitation strategy for restrictions and uncontrolled compensation

Translation

Range

Uncontrolled movement

(UCM)

The UCM may be uncontrolled translation, i.e. it is associated with laxity of joint connective tissues and aberrant recruitment of local stabilizer muscles, resulting in an abnormal control of translation and displacement of the PICM at an articular segment.

The UCM may be uncontrolled range, i.e. it is associated with excessive length or inefficient recruitment of global stabilizer muscles, resulting in increased relative flexibility.

Articular

Myofascial

Restriction

The restriction may be articular, i.e. it is associated with a lack of mobility of the joint and its connective tissues (e.g. capsule), resulting in an abnormal decreased translation and displacement of the PICM at an articular segment.

The restriction may be myofascial, i.e. it is associated with a lack of extensibility of contractile myofascial tissue (especially global mobilizer muscle) or neural tissue, resulting in increased relative stiffness.

As well as dealing with mechanical components of movement dysfunction, the pathology must be addressed and non-mechanical issues identified and managed (Figure 63.13) (Comerford and Mottram 2001b, 2012). Fitness and exercise programmes have been shown to be an effective treatment approach for chronic LBP (Frost et al. 1998; Torstensen et al. 1998). Consideration of psychosocial factors is essential in the management of LBP (Kendall and Watson 2000; Main and Watson 1999; Watson 2000; Watson and Kendall 2000). Cognitive behavioural approaches have a significant role in the management of chronic LBP (Klaber Moffet et al. 1999; Waddell 1998; Watson 2000).

Figure 63.13 Model of rehabilitation

Figure 63.13
Model of rehabilitation

(reprinted with permission from Movement Performance Solutions).

A useful guide for rehabilitation has been described using four principles of low load movement and stability rehabilitation (low threshold stability training) (Comerford and Mottram 2001b, 2012) (Table 63.11).

  • Principle I: Control of the site and direction of UCM

  • Principle II: Local control of translation in neutral position

  • Principle III: Global stabilizer control through range

  • Principle IV: Global mobilizer extensibility

Table 63.11 Principles of movement control retraining

Principle I:

Control of site and direction of UCM

Retrain control of the movement control impairments in the direction of symptom producing movements. Use the low threshold recruitment to control and limit motion at the segment or region of UCM and then actively move the adjacent restriction. Only move through as much range as the restriction allows or as far as the UCM is cognitively and efficiently controlled.

Principle II:

Local control of translation in neutral position

Retrain low threshold activation of the local stabilizer muscle roles to increase muscle stiffness and control intersegmental displacement in the neutral training region.

Control of recruitment synergy imbalance

Principle III:

Global stabilizer control through range

Retrain the global stabilizer muscle roles to actively control the full available range of joint motion. These muscles are required to be able to actively shorten and control limb load through to the full passive inner range of joint motion against gravity. They must also be able to control any hyper-mobile outer range. The ability to control rotational forces is an especially important role of global stabilizers. This is optimized by low-effort, sustained holds in the muscle’s shortened position with controlled eccentric lowering.

Principle IV:

Global mobilizer extensibility

When the two-joint global mobilizer muscles demonstrate a lack of extensibility due to up-regulation or adaptive shortening, compensatory overstrain or UCM occurs elsewhere in the movement system in an attempt to maintain function. It becomes necessary to lengthen or inhibit over-activity in the global mobilizer muscles to eliminate the need for compensation to keep function.

Once these four principles have been achieved, an additional three principles of high threshold (‘core’) stability training can be integrated into high load function (Comerford and Mottram 2014).

  • Principle V: Control during overload training

  • Principle VI: Control during slow spinal and girdle movements

  • Principle VII: Control during high-speed movements

This chapter will not detail these last three principles of high threshold ‘core’ stability.

Principle I: Control of the site and direction of UCM

The key goal to effective retraining is to re-establish control of the UCM and regain normal mobility of motion restrictions. The direction control tests that diagnose the site and direction of UCM can also become the retraining strategies. The aim is to change the recruitment pattern and actively control movement at the site and in the direction of stability dysfunction (Comerford and Mottram 2001b, 2012, 2014).

This is a process of sensory motor re-programming. For example, if the movement control impairment is diagnosed as lumbar flexion UCM, the therapist would instruct the subject actively to control or prevent lumbar flexion (while using visual and palpation feedback) while bending forwards independently at the hips (hip flexion) (e.g. Figure 63.3) or while lowering the thoracic spine into flexion independently of any lumbar movement. The movement control retraining focuses on the joint region where the movement is actively being controlled or limited (lumbar flexion), not the joint that is producing the movement (hip flexion or thoracic flexion) that is challenging the ability to control the UCM. This involves active cognitive recruitment of the lumbar extensor stabilizer muscles to isometrically control lumbar flexion during slow repetitions of the exercise. The flexion movement at the hip or the thoracic spine creates a flexion loading challenge that the lumbar extensor stabilizer muscles have to continually work against.

Worsley et al. (2013) have demonstrated the clinical effectiveness of using this process in patients with shoulder impingement pathologies. They measured significant shoulder pain and disability, failure of a scapula movement control test, aberrant scapula muscle recruitment (both delayed onset of activation and early termination of recruitment of the serratus anterior lower trapezius muscles) during arm movements, and altered scapula kinematics (reduced upward rotation and backward tilt) during arm movements. They showed that a 10-week movement control retraining programme, using scapular direction control retraining, achieved significant improvements in pain and disability, correction of movement control impairment, recovery of scapula muscle recruitment (onset of activation in termination of recruitment) to match normal controls, and recovery of normal scapula kinematics (increased upward rotation and backward tilt).

Another example of direction control retraining is for cervical rotation UCM where the subject needs to regain control of pain provocative cervical rotation (Figure 63.2). Position the cervical spine and scapula neutral, and rotate the head through the available range without substitution strategies (lateral flexion and chin poke). It may be useful to passively unload the ipsilateral scapula (taping, passive support). As range improves and symptoms decrease, the patient should begin to actively control the scapula position. This exercise can be started in a sitting position with support but should be progressed into function.

The sitting and standing bow tests can be used to retrain lumbar spine flexion stability dysfunction (Figures 63.3 and 63.4). The bent knee fallout test (Figure 63.5) can be used to retrain lumbo-pelvic rotation UCM.

Key points for rehabilitation

Retrain control of the site and direction of UCM:

  • Specific recruitment and control exercise programmes need to be practised to restore normal muscle function (Comerford and Mottram 2001b, 2012; Sahrmann 2000).

  • Control the UCM and move the restriction.

  • Use conscious activation of the stability muscles to control or prevent the provocative movement and move the adjacent joint or motion segment.

  • Movement at the adjacent joint should be independent of the region of poor movement control.

  • Movement must be controlled eccentrically as well as concentrically.

  • Move at adjacent joint only as far as:

    • control of the UCM can be maintained

    • the restriction at the adjacent joint allows.

  • Try to use low to moderate effort to facilitate tonic recruitment. Maximum effort (co-contraction rigidity) is to be discouraged.

  • The movement control impairment is direction-dependent and relates to the type and nature of pathology.

  • Direction control movements are not stretches or strengthening exercises: Low force! No stretch! No strain! No substitution! No fatigue! No pain!

Principle II: Local control of translation in neutral position

Retraining the local stabilizer muscles to recover their low threshold recruitment and timing deficiencies in order to regain control of inter-segmental displacement or translation requires specific activation of the local stabilizer muscles, without substitution strategies. There is evidence that the transversus abdominis is controlled independently of other abdominal muscles (Hodges and Richardson 1999). The contraction needs to be sustained with the joint in neutral position and under low physiological load, independently of normal related reading and without movement (substitution with the global muscle system). The emphasis here is on motor control and recruitment and not strength and flexibility. The goal is to regain the normal automatic recruitment and timing of the local stabilizer muscle roles for the lumbar and cervical spines.

Teaching the specific activation of the local stability muscle role requires good clinical observation and instruction skills from the therapist. Local muscle retraining often requires specific facilitation techniques as appropriate (Figure 63.14) (Comerford and Mottram 2012, 2014). Facilitation techniques will help to improve proprioceptive awareness and cognitive activation, thus assisting in recovery of low threshold, slow motor unit recruitment.

Figure 63.14 Specific recruitment of the local stability system

Figure 63.14
Specific recruitment of the local stability system

(reprinted with permission from Movement Performance Solutions).

Re-education of the local stabilizer role of the deep neck flexors requires the patient to learn a pure head nodding action (cranio-cervical flexion), which the clinician must carefully teach (Jull 1998; Jull et al. 2000). The gentleness and precision of the action needs to be reinforced. The aim is to train 10-second holds, with 10 repetitions, with the appropriate pressure change (Jull 1998) (Figure 63.6). As control and recruitment improves, the ability to sustain the optimal pressure change without substitution ‘feels easy’.

The specific activation of the transversus abdominis is taught by asking the patient to gently draw in (hollow) the low abdominal wall (Hodges et al. 1996; Richardson and Hodges 1996; Richardson and Jull 1995; Richardson et al. 1999, 2004) (Figure 63.7). Facilitation and learning techniques can be employed to assist the patient. These include visualization and instructional cues (e.g. ‘draw your lower abdomen up and in’ to encourage conscious activation), tactile feedback, breathing control, and facilitation through a pelvic floor contraction or multifidus co-activation. Any facilitation through co-activation of other muscles should ideally be a short-term option, with specific cognitive activation using visual and palpation feedback being a preferable strategy.

Recruiting a sustained and repeatable multifidus contraction needs specific instruction (Hides et al. 1996) (Figure 63.8). Again, visualization and cues are useful facilitators, as is achieving a joint neutral spinal position (Hamilton 1998; Richardson et al. 1999).

The re-education of the local stabilizer role of the psoas major involves the action of longitudinal compression; for example, ‘shortening the leg’ or attempting ‘to pull the hip into the socket’. Psoas contraction should increase stiffness segmentally in the lumbar spine and should resist motion segmentally rather than produce it. Optimal facilitation and retraining requires providing an appropriate low load facilitation and feedback. This training is best started in supine, side-lying, or inclined sitting position before progressing into function. Useful facilitation techniques are co-activation with the pelvic floor, breathing control, and low effort lateral rotation of the femur (Comerford and Mottram 2012, 2014). During active retraining of the psoas, it is also essential to identify and eliminate various substitution strategies and faults.

The patient must at all times be able to maintain consistent specific recruitment of the local stabilizer muscle from their breathing pattern. Subjects with back pain have demonstrated difficulty dissociating respiration from recruitment of the lumbar stability muscles (Cairns et al. 2000; Richardson et al. 2004). Once activation has been achieved in the clinic, the patient needs to practise so that the motor control pattern becomes integrated into all functional positions (see Box 63.1) (Comerford and Mottram 2012, 2014).

O’Sullivan et al. (1997a) have demonstrated the clinical effectiveness and importance of the integration of the deep stability muscle system into functional movements, activities of daily living, and even to high loads and provocative positions.

Key points for rehabilitation

Activation of local and global stability muscles to control the neutral joint position:

  • Specific activation of the deep local stability muscles in the neutral joint position.

  • The contraction is biased for the local stability muscles.

  • The contraction is isometric.

  • The contraction should be biased for slow motor unit recruitment (low force).

  • It is a conscious activation requiring motor planning and proprioceptive feedback.

  • The ability to sustain a consistent low force hold is paramount for rehabilitation of motor control deficits.

  • Optimal facilitation is dependent on identification and elimination of substitution strategies and overload or fatigue.

  • A high sensation of effort is permissible initially, but as control and functional integration return, a low sensation of effort activation should dominate.

  • There should be no fatigue or substitution.

  • Recruitment of the stability muscles to control the joint neutral position must be non-provocative and pain-free.

  • Low threshold motor control retraining is the intention—not strength training.

Principle III: Global stabilizer through range control

When spinal stability can be maintained during movements of the limbs into flexion, extension, rotation, or abduction, then the global stability muscles can be retrained to achieve through-range control. Global stabilizer muscles are designed to be the dominant synergist producing and controlling motion during non-fatiguing functional movements and postural control tasks. Muscles with a global stabilizer role are therefore required to have the ability to:

  • Concentrically shorten to synergistically contribute to joint motion in the full physiological inner-range position with no greater resistance than limb load against gravity, without substitution of the global mobilizer synergists.

  • Isometrically hold this (or any other) position to sustain postural alignment or support functional trunk or limb load.

  • Eccentrically control the return through range (limb lowering against gravity). The muscles are required to eccentrically control or decelerate rotational strain at all joints, especially the trunk and girdles. They should contribute significantly to rotation control in all functional movements.

  • Control whatever functional range is available. Therefore, the global stabilizers should demonstrate efficient control of both normal and hypermobile ranges of motion.

There are five key elements to retraining the global stabilizer muscles to produce and control non-fatiguing range of motion (Comerford and Mottram 2012, 2014):

  1. 1 Retrain low threshold recruitment (low force/low load exercise). The stabilization force must be low actual effort—in the range of less than 30% of maximum voluntary contraction (MVC) to ensure efficient recruitment of low threshold slow motor units for non-fatiguing function.

  2. 2 Retrain holding time. Increasing the holding time of muscle activation aims to facilitate low threshold slow motor unit recruitment. The ability to sustain this contraction seems to be important for prevention of recurrence and for return of function (Hides et al. 1996; Hodges and Richardson 1996; Richardson and Jull 1995; Richardson et al. 2004). Optimal holding times may vary but the general clinical guide is of a 10-second, consistently sustained contraction, repeated 10 times.

  3. 3 Retrain the muscle’s shortened position (inner-range hold) to increase force efficiency in ranges of postural control. The low-force, sustained contractions ideally should be performed in the muscle’s shortened range, and at the point that can be comfortably held for 10 seconds, to facilitate muscle inner-range control and recovery of low threshold recruitment.

  4. 4 Retrain eccentric control muscle lengthening, especially during limb lowering against gravity. The eccentric control of the active movement from the muscle’s shortened position is important to retrain as part of the low-force, sustained hold. Poor eccentric control is commonly observed clinically. Eccentric control of the outer range of movement is especially important for movement control. If hypermobile range of motion is evident, eccentric control of that range has high priority.

    Through-range control of the cervico-thoracic stabilizing extensors (semi-spinalis) is required to produce controlled low survival extension and rotation into shortened range and to eccentrically control the low cervical flexion through range (Figure 63.9). When movement is performed correctly (without substitution or fatigue), the range that can be controlled actively equals the available passive range of cervical extension.

  5. 5 Retrain the global stabilizer muscle’s holding time to the point that through range can be controlled without substitution (ideally, 10-second hold for 10 repetitions).

    Through-range control of the hip stabilizing extensors (gluteals) is required to produce controlled hip extension into shortened range and eccentrically control hip flexion through range. The patient supports their trunk on the edge of a bench, table, or bed with both feet supported on the floor and the knees slightly flexed. The lumbar spine is positioned in neutral alignment. The abdominal and gluteal muscles are co-activated to control the neutral spine and to prevent excessive lumbar extension. The patient is instructed to bend one knee to 90° and then lift that bent leg into hip extension. The hip extension must be independent of any lumbo-pelvic motion. The leg is extended only as far as the neutral lumbo-pelvic position can be maintained without cramping or over-activation of the hamstrings. At this point, the leg is slowly lowered back towards the floor. Initially, the patient may only be able to dissociate the lumbar spine (neutral) from hip extension to within 40°Flexion from horizontal.

    As the ability to control lumbo-pelvic extension gets easier and the pattern of dissociation feels less unnatural, the exercise can be progressed to hip extension level with the horizontal (0°) and, eventually, to 10–15° of extension above the horizontal. When the patient can lift the leg horizontal (to 0° hip extension), and control lumbo-pelvic neutral position, the exercise can be progressed in prone position (Figure 63.10). The patient is positioned prone with a pillow under the pelvis (hips flexed to approximately 10–15°) to allow the gluteals to work from an efficient length. The subject is instructed to bend one knee past 90° (to relax the hamstrings) and then lift that knee (hip extension) approximately 3 to 5 cm (1 to 2 inches). The leg may lift into extension only as far as the neutral lumbo pelvic position can be maintained without cramping or over-activation of the hamstrings. At this point, the leg is slowly lowered back towards the floor while also maintaining the lumbo-pelvic neutral position.

Key points for rehabilitation

Low threshold recruitment, through-range control of the global stability muscles:

  • Low force to encourage slow motor unit recruitment.

  • Increasing the holding time of muscles that have a stability function has priority over strengthening. This is to facilitate recruitment of tonic fibres and train specificity of anti-gravity holding function.

  • Shortened muscle position—a basic requirement of stability function is that the global stabilizer muscles have the ability to move the limbs (functional load) through their available range; or at least move the limbs through the same range that the synergistic global mobilizers can.

  • Eccentric control is important to control the joint through range.

  • The rotatory component of global stabilizer muscle action must be controlled during the low-force, sustained hold. Therefore, it is important to have reasonable rotation direction control ability prior to retraining the global stabilizer function.

  • Exercise in a closed kinetic chain environment (distal fixation or weightbearing) allows better low threshold recruitment and also provides additional proprioceptive afferent information.

  • No phasic recruitment or dominance of global muscles should be allowed.

Principle IV: global mobilizer extensibility

The global mobility muscles with centrally mediated up-regulation and over-activity have also frequently lost extensibility. There is a need to inhibit or down-regulate their excessive tonic, slow motor unit recruitment and to regain their ideal physiological length and extensibility. There are many appropriate techniques that can be employed to achieve this goal, e.g. inhibitory muscle lengthening, soft tissue techniques, and myofascial release. Rehabilitation should ensure that these multi-joint global mobilizers are not the dominant synergists for non-fatiguing functional movements and postural control tasks (Comerford and Mottram 2012, 2014). Their primary role is for high-load/high-speed activity.

Key points for rehabilitation

Regain extensibility and inhibit the short or over-active global mobility muscles:

  • The aim here is to target the tight tissue, and techniques can be used to address the tight contractile or connective tissue. Techniques for regaining length and inhibition of over-active muscles include myofascial release, proprioceptive neuromuscular facilitation, muscle energy techniques, and active inhibitory restabilizations.

  • An inhibitory lengthening technique, ‘active inhibitory restabilization’, is a useful technique for regaining length. It involves the operator gently and slowly lengthening the muscle until the resistance causes a slight loss of proximal girdle or trunk stability (into the stability dysfunction). The operator then maintains the muscle or limb in this position. The subject is then instructed to actively restabilize the proximal segment that has lost stability and sustain the correction for 20–30 seconds, repeat this 3–5 times. This encourages reciprocal inhibition of the over-active muscle and bonus proximal stability (Figures 63.11 and 63.12).

None of the corrective exercises to directly improve dynamic stability (Principles I, II, and III) should produce or provoke any symptoms at all. If any symptoms are aggravated or provoked by corrective exercises, first check that the exercise is being performed correctly, with appropriate low load and control. Overload is the most common cause of provocation. If an appropriate exercise is performed correctly but is still provocative, then other issues must be considered—acute inflammatory pathology, gross segmental instability, neurogenic or neuropathic pain, visceral pain, or serious medical pathology.

Conclusion: movement control impairments

There is a growing volume of evidence which suggests that improving muscle recruitment strategies and thresholds to restore ideal function, by assessing and correcting movement control impairments, is an integral part of the management of patients presenting with spinal pain of neuromusculoskeletal origin. Research evidence shows that patients with LBP may demonstrate movement control impairments in both the local and global stability systems, resulting in uncontrolled movement which can be diagnosed in terms of the site and direction of cognitive movement control deficiencies. Local muscle role impairments present as a change in the recruitment of the deep local stability muscles that have a role in maintaining dynamic stability at the spinal motion segments. Global movement control impairments present as a lack of global muscle control of direction, especially rotation, but also flexion, extension, and other directions. Global stabilizer muscle impairments also present as an imbalance in the recruitment thresholds and strategies between the one-joint global stabilizer and multi-joint global mobilizer synergists. The global stabilizer synergists demonstrate central down-regulation and inhibition, contributing to a lack of efficiency of through-range control of joint motion and poor low threshold postural recruitment. The global mobilizer synergists demonstrate central up-regulation and a loss of myofascial extensibility, together with inappropriate dominance of low threshold postural function. These changes are associated with the presentation of spinal pain, disability, and movement control impairments (Figure 63.15).

Figure 63.15 Movement dysfunction model

Figure 63.15
Movement dysfunction model

(reprinted with permission from Movement Performance Solutions).

Assessment procedures and rehabilitation strategies for retraining movement control impairments in regaining control of the site and direction of UCM have been described (Comerford and Mottram 2001a,b, 2012; Richardson et al. 1999, 2004) and there is evidence of effectiveness for movement control retraining programmes (Beeton and Jull 1994; Grant et al. 1997; Hides 1998; O’Sullivan et al. 1997a, 1998).

The ability to assess movement function and correct movement control impairments is a key clinical skill required when managing neuromusculoskeletal pain and dysfunction. Evidence suggests that therapists would benefit from having the skills to assess for UCM and rehabilitate movement control impairments in patients attending the clinic with spinal pain, both acute and chronic.

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