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Muscle imbalance in neurological conditions D Fitzgerald

M Stokes

INTRODUCTION CHAPTER CONTENTS Introduction 501 Theoretical basis of muscle imbalance 502 Global and local muscle systems 502 Evidence for specific postural muscle function 503 Causes of muscle imbalance 504 Physiological consequences of altered muscle function 504 Mechanical consequences of altered muscle function 504 Neurophysiological aspects of altered muscle function 507 Biochemical consequences of altered muscle function 507 Assessment of muscle imbalance 508 Postural alignment 508 Muscle length 509 Muscle strength 509 Holding capacity (endurance) 511 Movement patterns 511 Correction of muscle imbalance 511 Retraining muscle activation 512 Restoration of muscle length 512 Restoring stability 512 Conclusions 512 Case history 512 References 513

Muscle imbalance is said to occur when relative changes in muscle length and recruitment patterns take place between agonist/antagonist and synergist muscle groups. The ratio of muscle strength and flexibility alters, and functional consequences include abnormal movement patterns, pain and instability. The concept of muscle imbalance has emerged from several different sources over the latter half of the twentieth century. The most noted contributors were Kendall & Kendall (1938), Lewitt (1991), Janda (1978), Klein Vogelback (1990), Bobath (1990), Carr & Shepherd (1999) and, more recently, Sahrmann (2002) and Richardson et al. (1999). The common ideology amongst these systems of approach is an attempt to quantify the efficiency of muscle activity during functional movement. All systems are largely derived from clinical practice and hypothesise regarding the efficiency of movement but also draw on an increasing body of substantive scientific data. Whilst it is acknowledged that the detail of our understanding of muscle control in functional movement is in its infancy, there is an accumulating evidence derived from biomechanics, neurophysiology, motor control and skill acquisition, together with basic sciences of muscle physiology, anatomy and human movement. Much of the analysis centres around evaluating the interaction between agonist, antagonist and synergist muscle activity. The clinical application of this approach is to optimise stress within the musculoskeletal system and prevent or treat regions where dysfunctional movement has produced tissue overload. These concepts are also used in an attempt to optimise movement patterns and hence functional efficiency.

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Table 30.1 Examples of muscles with a mainly postural or dynamic function Mainly postural function

Dynamic function (phasic)

Stenocleidomastoid Pectoralis major Trapezius Levator scapulae

Scaleni Pectoralis major Subscapularis Extensors of the upper extremity Trapezius

Flexors of the upper extremity Quadratus lumborum Back extensors Hip flexors Lateral hip rotators Medial hip rotators Hamstrings Plantarflexors

Rhomboids Serratus anterior Rectus abdominis Obliquus abdominis externus Obliquus abdominis internus Gluteus minimus, medius and maximus Vastus medialis and lateralis Tibalis anterior Peronei

THEORETICAL BASIS OF MUSCLE IMBALANCE Kinetic data (forces and movement causing motion) and kinematic data (analysis of body segment motion) are the scientific methods used to measure human function (Durward et al., 1999). Notwithstanding the impressive developments in this area, there are significant technical limitations in the ability to determine the precise interaction between multiple muscles involved in a movement and the distribution of stress within the system. Consequently, clinicians developed a battery of tests involving components of: ● ● ●

functional movement patterns isolated muscle strength tests isolated muscle flexibility tests.

These three components are the essential elements of applying muscle imbalance concepts in clinical practice. Initial clinical observations (Janda, 1983; Lewitt, 1991) suggested characteristic alterations in muscle function associated with variation in postural alignment. Essentially some muscles show a tendency to shorten and become hyperactive, and some muscles show a tendency to lengthen and become inhibited. Examples of these muscles are outlined in Table 30.1. These observations were initially made in patients who had lesions of the central nervous system (CNS), who developed characteristic postural deformities associated with changes in muscle tone (both hyper- and hypotonicity). This clinical subgroup constitutes the

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most extreme end of the muscle imbalance spectrum, whilst non-CNS lesion cases represent the other end of the clinical spectrum, displaying similarities in movement pattern disturbance without gross neurological disruption. Attempts to determine the underlying mechanism have speculated a relationship to muscle fibre-type characteristics, muscle morphology, phylogenetic characteristics and muscle architecture, but without consensus. At present, it seems unlikely that any of these hypotheses offers a complete explanation of clinical observations.

Key points Possible underlying mechanism of muscle imbalance: ● Muscle fibre-type characteristics ● Muscle morphology ● Phylogenetic characteristics ● Muscle architecture No consensus has yet been reached

The assessment of muscle in relation to movement dysfunction takes into account the anatomical, biomechanical, physiological and biochemical properties of the muscles, and the motor control patterns in which they operate. Precise classification of muscle into postural or phasic characteristics is not always possible and leads to confusion reviewing literature, which classifies muscle according to putative function. Problems with terminology arise if the terms ‘postural’ and ‘phasic muscles’ are used, as the two systems no longer appear to concur, due to Janda’s altered meaning of the words. Some conflicts include tensor fascia lata, hamstrings and gastrocnemius, which are movement synergists in one classification (Richardson, 1992) and postural muscles in the other (Jull & Janda, 1987). Inconsistencies are less apparent if muscle length (short/hyperactive, lengthened/inhibited) concepts are applied and it may help to bear this in mind when reading any literature by Janda or any reviews which mention this classification (Norris, 1995a).

Global and local muscle systems It is known that the neuromuscular system employs complex and varying strategies of cocontraction to provide stiffness and stability during functional movement (Pope et al., 1986; Roy et al., 1989; Lavender et al., 1993a, b; Thelen et al., 1995; O’Sullivan & Taylor, 2000). Stability is required to produce movement about a controlled axis and to equilibrate moments created at other joints as a consequence of motion. This has led to

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Table 30.2 Features of the upper motor neurone (corticofugal) syndrome NEGATIVE Acute hypotonia (shock) Weakness due to inadequate muscle activation Loss of dexterity Loss of cutaneous reflexes Fatiguability POSITIVE At rest, in response to peripheral stimulation Proprioceptive Nociceptive Increased tendon reflexes Positive Babinsky with radiation Extensor spasms Clonus Flexor spasms Spasticity Mass reflex During movement (spastic dystonias) Dyssynergic patterns of co-contraction Associated reactions Flexor withdrawal reflexes Positive support reaction Extensor thrust ‘Pushing’ reactions Adapted from Greenwood (1998), with permission.

the concept of global and local muscle systems (Bergmark, 1989). The global muscle system consists of large torque-producing muscles that act upon the region they cross, without having direct anatomical attachments to the area. The local muscle system consists of deep, local muscles positioned close to the joint axis, inserted into adjacent segments and producing significant compressive force components, as opposed to torque. This concept has provided a framework for much of the contemporary research into muscle imbalance, particularly with regard to the spine and pelvis (Richardson et al., 1999). There is some experimental evidence to support the stability/mobility concept in normally functioning muscles, in that rapid movements which mainly involve type II muscle fibres have been shown selectively to recruit mobility muscles and conversely inhibit synergic stabilising musculature. Examples include: rapid knee extension involving greater rectus femoris activity than vastii activity (Richardson & Bullock, 1986); rapid ankle plantarflexion producing greater activity and a training effect in gastrocnemius rather than soleus (Ng & Richardson, 1990); rapid trunk flexion involving greater activity of rectus abdominis than the oblique abdominal muscles (Thorstensson et al., 1985; Wohlfahrt et al., 1993); and, in cyclists, lengthening and reduced activity of gluteus

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maximus (Richardson & Sims, 1991). Richardson (1992) suggested that the movement synergists take over a stability role, as the stability synergists are activated less than the movement synergists. Since the stability synergists are thought to be used less in muscle imbalance syndromes displaying a tendency to lengthen, presumably by reduced tonic activity and increased phasic activity reducing endurance, the movement synergists become more active and increase their tonic activity to take over the stabilising role of the joints. In the neurologically impaired patient the application of these concepts is confounded by pathology which affects the spinal or upper motor neurone pools. This pathophysiology results in alterations in muscle tone (either increases or decreases) and consequent disturbances in movement, as outlined in Table 30.2 (Greenwood, 1998).

Evidence for specific postural muscle function Much of the scientific investigation has been directed towards the lumbopelvic region (Richardson et al., 1999) but there are also data accumulating for the cervical spine, shoulder girdle, knee and ankle, as discussed below. Cresswell et al. (1992) initially observed continual activation of transversus abdominis, regardless of the direction of trunk motion. Other trunk musculature showed variations in activity, predictable from the direction of displacement. Multifidus, lumbar longissimus and illiocostalis showed sustained activation in upright postures such as standing and walking (Richardson et al., 1999, Ch. 3). Whilst muscles such as lumbar multifidus can provide up to two-thirds of the control of intersegmental motion in certain directions (sagittal plane), it is limited in its ability to control rotation (Wilke et al., 1995). Therefore co-ordinated patterns of muscle recruitment are essential between the global and local muscle systems of the trunk in order to compensate for changing demands of daily life and to ensure that the dynamic stability of the spine is preserved (Gardner Morse et al., 1995; Cholewicki et al., 1996). Co-contraction between transverse abdominis and lumbar multifidus has been observed in static postures and dynamic movements of the spine (Cresswell et al., 1992, 1994). Increasing levels of postural load are associated with an increase in co-activation of both global and local muscle systems to meet the increasing demands (McGill, 1992). Increasing the speed of dynamic load has been shown to increase the recruitment of postural stabilising muscles and influence their level of activity (Cresswell et al., 1994; Hodges, 1999).

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The evidence for neuromuscular dysfunction has come from investigating patients with low-back pain. These observations primarily relate to disturbances in the pattern of muscle recruitment and the co-contraction between different muscle synergies. The types of changes observed relate to delayed/absence of firing, inappropriate increase in muscle co-contraction enhancing stiffness and impaired anticipatory/ feedforward motor relegation (Hodges, 1999; O’Sullivan & Taylor, 2000). Deficits in control of the neuromuscular system have also been noted in subjects with functional shoulder instability (Lephart et al., 1993; Sainburg et al., 1993) and shoulder impingement syndromes (Pink, 2000). Knee patients with anterior cruciate ligament deficiencies show disturbed firing patterns between quadriceps and hamstrings in specific ranges of the gait cycle and different patterns of activation under functional load (Andriacchi, 1990; Noyes et al., 1992). Subjects with chronic ankle instability also display impaired joint stability (Gottlieb et al., 1996), impaired proprioceptive function (Jerosch & Bischof, 1996) and alterations in contraction timing (Lynch et al., 1996). From the above overview it is evident that the debate has moved beyond issues of strength and flexibility, which have historically been the focus of rehabilitation research. The focus of critical research now includes issues regarding: ● ●

the recruitment, co-ordination and regulation of muscle activity together with feedforward/feedback control mechanisms during functional tasks.

We also require greater understanding of: ●

●

the observed alterations in muscle control outlined above, particularly the cause-and-effect relationship in the pathological process the variability in motor control of movement patterns in order to determine the clinical significance of these variations and whether they represent legitimate targets for rehabilitation.

Key points ● ● ●

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The debate has moved beyond strength and flexibility Motor control mechanisms during functional tasks are now the focus of research in rehabilitation Need to determine the clinical significance of variability of motor control in movement patterns

CAUSES OF MUSCLE IMBALANCE Several factors have been suggested as causes of muscle imbalance, based on clinical observation (reviewed by Norris, 1995a): ● ● ●

● ●

habitual poor posture and alignment problems (Sahrmann, 2002) pain may lead to postures that reduce pain but cause imbalance and abnormal alignment joint pathology can cause reflex inhibition of muscle activity, which tends to inhibit selectively certain muscles associated with a joint (Stokes & Young, 1984) and may therefore lead to imbalance muscle imbalance has been suggested as a cause of injury (Grace, 1985) modern lifestyle activities at work and in sport may lead to muscles changing their activation pattern and thus functional role, therefore leading to imbalance (Richardson, 1992).

Clearly, any of these causal factors can become involved in a vicious cycle in which it may not be possible to state which came first, i.e. imbalance, altered length, strength or recruitment, or injury.

PHYSIOLOGICAL CONSEQUENCES OF ALTERED MUSCLE FUNCTION The strength and excitability of a muscle alter with changes in length (Sahrmann, 1987, 2002). The effects of variation in resting muscle length can be considered in biomechanical, neurophysiological and biochemical terms.

Mechanical consequences of altered muscle function The most obvious implications of changing muscle length relate to musculotendinous shortening with reduced elasticity, resulting in compromised available range of motion or increased tensile load induced by changes in the associated joint kinematics. A typical example of this relates to hip flexor tightness associated with increased lumbar lordosis and anterior pelvic tilt. The mechanical consequences of hip flexor tightness are to interfere with the normal mechanics of hip extension. Moderate tightness may not produce an overt restriction in hip extension range but manifest itself as anterior hip pain as a consequence of increased tissue load. Soft-tissue adaptations initiate progressive loss of elasticity in association with impairment of joint motion. These adaptive changes relating to changes in muscle fibre length are well recognised from studies

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Changes in muscle tissue The length/tension relationship for muscle defines the ability of a muscle to generate force as a consequence of its length. The length/tension relationships have been shown to alter due to changes in muscle length (Williams & Goldspink, 1978; Goldspink & Williams, 1990).

Changes in fibre length It has been demonstrated that lengthened muscles gain sarcomeres and shortened muscles lose sarcomeres, with normal sarcomere numbers being restored when immobilisation is discontinued (Williams & Goldspink, 1978; Goldspink & Williams, 1990; Thompson et al., 1998; Thompson, 2002). Changes in fibre diameter Muscle shortening can also occur without loss of sarcomeres. Fibre length was not reduced in the gastrocnemius muscles of children with spastic diplegia and plantarflexion contractures (Shortland et al., 2002). Extrapolating from the findings of animal studies, where fibre length was normal but diameter was reduced, the investigators concluded that muscle shortening was due to fibre atrophy; the proposed mechanism is loss of muscle fibre diameter in pennate muscles causing shortening of the aponeuroses, thus shortening the muscle and leading to contracture. Although only indirect evidence was provided for atrophy producing shortening, the contractures seen in the children studied could not be explained by sarcomere loss. This phenomenon needs to be studied in other disorders. It may transpire that, in certain conditions, loss of both fibre diameter and length coexist. The clinical implications of this observation, regarding muscle strengthening as a means of treating and preventing contractures, are discussed in Chapters 25 and 29.

Effects on function The effect of these adaptations to muscle length on physiological function is to cause a shift in the length/tension relationship (Fig. 30.1). In lengthened muscles, the curve is shifted to the right so that peak tension occurs at a longer length than normal (in the position in which it has been immobilised). Also, because the muscle is longer and has a greater mechanical advantage, its absolute peak tension is greater that that of a muscle of normal length. In the shortened muscle, the curve is shifted to the left of

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Active tension (g)

assessing the effect of immobilisation/postsurgical interventions (Thompson, 2002), and from muscle length-testing protocols (Janda, 1983; Kendall et al., 1993). The more recent concept of muscle fibre atrophy causing shortening (Shortland et al., 2002; discussed below) has yet to be explored in rehabilitation research.

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Shortened Control Lengthened

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A

6 4 2

B

80 90 100 110 Muscle belly length as a percentage of optimal length

Figure 30.1 Changes in the length/tension curve for muscles immobilised in lengthened and shortened positions. (Redrawn from Norris (1995a), adapted from Gossman et al. (1982), with permission.)

normal, giving a lower peak tension. Therefore, the normal length/tension relationship for individual muscles applies to situations where sarcomere number remains constant and sarcomere number corresponds to anatomical muscle length parameters. The spontaneous return to normal sarcomere number following the removal of external constraints suggests a physiological mechanism to restore homeostasis and optimal muscle mechanics. From Figure 30.1 it can be seen that lengthened muscles are stronger that normal and shorter muscles are weaker than normal when tested at their optimal length; this can be achieved under laboratory conditions. The optimal length of a lengthened muscle (point A in Fig. 30.1) can produce a peak tension which is up to 35% greater than that of a muscle of normal length (Williams & Goldspink, 1978). However, consider a muscle tested in inner range, which is approximately just over 80% of the optimal length for a muscle of normal length (point B in Fig. 30.1). At this point of the range, optimal length is not achieved for any length of muscle and favours greatest tension in the shortened muscles. This is because in inner range, the myofilaments of the lengthened muscle would overlap excessively, with redundant cross-bridge formation and a consequent reduction in power output. Under clinical conditions, therefore, lengthened muscles appear weaker than short muscles (length/ tension adaptive changes), particularly if tested in neutral anatomical positions (mid or inner range). It is therefore imperative in clinical testing that muscle strength should be assessed throughout its operational range and not just in one anatomical position.

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Key point

Biomechanically, the function of the scapula is to rotate the glenoid upwards during arm elevation and this is primarily accomplished by scapular protraction and upward rotation, producing movement of the inferior angle around the chest wall. The force couple is generated by upper and lower fibres of trapezius and serratus anterior, while middle trapezius and rhomboids act to stabilise the scapula on the thorax. A tendency for superior scapular migration during this movement pattern implies that the upper trapezius is more dominant in the synergy. Whether the cause is primary trapezius hyperactivity or weakness or inhibition of lower trapezius and serratus anterior, the therapeutic goal is to reduce or diminish the tendency for superior scapular migration. This can be achieved by the therapist either applying a downward force on the scapula as the motion occurs in order to give feedback or by prescribing specific scapular stabilisation exercises (Bryden & Fitzgerald, 2001), if adaptive changes have occurred in the upper limb, i.e. biceps. In summary, the physiological consequences of alterations in muscle length produce increasing discrepancy between the joint angle, giving rise to optimal muscle torque and the normal joint mechanics. In practical terms this means that, for example, the lengthening produced in middle and lower trapezius as a consequence of upper-limb spasticity effectively changes a neutral scapular alignment to an inner range of motion for these muscles. Similar analogies apply to a lengthened gluteus maximus associated with tight hip flexors, or a lengthened anterolateral abdominal wall associated with a sway-back posture.

Clinical testing

Connective tissue changes

Figure 30.2 Superior scapular migration (left) indicative of alteration in synergic control of scapular position on thorax. There is dominance of the scapular suspensory muscles.

Strength should be assessed throughout the operational range of a muscle and not just one anatomical position

If muscles are incapable of generating force throughout their operational range, then either range of motion will be impaired or compensatory movement strategies will be employed to achieve functional range. This compensatory movement strategy is considered to be a typical finding in muscle imbalance syndromes and an example in the shoulder may serve to illustrate. Assessing the pattern of scapular motion during arm elevation can yield useful information regarding the synergic function of scapular muscles (Janda, 1983; Lewitt, 1991; Culham & Peat, 1993). When evaluating arm elevation, the therapist monitors the contour of the upper trapezius and the tendency for superior scapular migration (Fig. 30.2).

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The physical changes in muscle length are associated with connective tissue adaptation. As described above, Williams & Goldspink (1973) demonstrated the addition and subtraction of sarcomeres to muscle fibres, depending on the position of immobilisation. There is a proliferation of extracellular connective tissue, with resultant increase in passive stiffness and muscle shortening (Lieber, 1992, Ch. 5). The remodelling of dense connective tissue can be considered in two phases – the initial gross disorganisation of unstressed collagen bundles (with associated weakness) evident within a few days of immobilisation (Enwemeka, 1990), and the second stage of remodelling producing consolidation of the randomly aligned collagen to form contracture (Cummings & Tillman, 1992). Ten weeks of connective tissue proliferation with resultant shortening has been shown to be fully reversible (Lieber, 1992) and clinical experience would suggest that it extends well beyond this point. However, determining the

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point at which contracture is irreversible is largely based on response to appropriate treatment techniques and may ultimately require surgical intervention.

Neurophysiological aspects of altered muscle function Preferential recruitment theory The suggestion made in this theory, that shortened muscles are recruited first in a movement pattern, was based on the clinical observations of Sahrmann (1987, 2002). The hypothesis suggests that the neural drive or gain is enhanced in physiologically shortened muscles, thus lowering the recruitment threshold and making them more dominant in a movement synergy. There is some evidence to substantiate this. Hodges & Richardson (1997a, b) have demonstrated a delay in recruitment of the transverse abdominis muscles in patients with low-back pain. Babyar (1996) demonstrated that patients with shoulder pain have excessive scapular elevation which persists in the absence of pain. Mueller et al. (1994) have shown that diabetic patients with impaired ankle dorsiflexion use a hipdominant strategy for walking.

Co-activation The co-activation of abdominal and hamstring muscles has been investigated, demonstrating that a decrease in activity of one muscle in a force couple is accompanied by an increase in activity of another (Mayhew et al., 1983). Richardson & Sims (1991) have shown reduced activation of the lengthened gluteus maximus in cyclists. This type of subtle alteration in the reciprocal participation of muscle synergies is thought to contribute to muscle imbalances by reinforcing the demands of a stronger muscle and minimising the demands of the weaker muscles (Sahrmann, 2002).

Proprioception Alterations in neuronal control profoundly influence the sensory input and motor control required for purposeful movement (Lephart & Fu, 2001). Historically, these issues have been considered as proprioception (Sherrington, 1906). In physiological terms, this requires many afferent receptors to convert mechanical stimuli into neural signals for CNS processing to produce controlled motor output. The current challenge is to understand the integration of these systems to provide the optimal treatment protocols. In neurologically impaired patients, a major clinical challenge is to achieve adequate limb alignment in order to approximate normal afferent input. This is an

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important distinction between rehabilitation which is purely focused on achieving functional objectives regardless of the muscle recruitment strategy (motor relearning theory), as opposed to ‘normal’ movement advocates (Bobath, 1990), who focus on optimising limb alignment and muscle tone as a prerequisite to rehabilitation of functional goals. The clinician has several therapeutic options to enhance proprioceptive function, such as using unstable surfaces, cutaneous stimulation around the muscle, verbal, visual or auditory feedback using mirrors or video, electromyogram (EMG) biofeedback or palpatory facilitation of the target muscles. In terms of motor control theory, there is a putative hierarchy of progression from cognitive activation to associative motor learning to autonomous (Shumway-Cook & Woollacott, 1995).

Pain associated with tightened muscles Painful trigger points, which are areas of hypersensitive tissue, can occur in shortened hyperactive muscles observed in myofascial pain syndromes (Travell & Simons, 1983). There is deep tenderness and increased tone (the so-called twitch response), which is palpable and easily demonstrated clinically. Each muscle has a characteristic pain referral pattern and can also mimic autonomic dysfunction or peripheral neuropathic pain. There is much debate regarding the pathophysiology of trigger points (Wall, 1993) but they are frequently demonstrable in high-tone patients and are amenable to a variety of treatment techniques, such as sustained pressure, stretching, coolant spray, soft-tissue massage or modalities such as laser or acupunture.

Biochemical consequences of altered muscle function Skeletal muscle adaptation through inactivity, therapeutic exercise, training and overload has been well investigated and reviewed (Lieber, 1992; Baechle & Earle, 2000). Adult skeletal muscle contains at least three distinct fibre types, classified because of their functional and metabolic properties as fast glycolytic (type IIa), fast oxidative glycolytic (type IIb) and slow oxidative (type I). Fast glycolytic and fast oxidative glycolytic fibre types are fast-twitch fibres, characterised by fast myofibrillar adenosine triphosphatase (ATPase) and sarcoplasmic reticulum calcium (Ca)-ATPase activities, and correspondingly short isometric twitch durations and fast maximal shortening velocities. In contrast, the slow oxidative fibre possesses slow sarcoplasmic reticulum Ca-ATPase and myofibrillar ATPase activities, prolonged twitch duration and slow maximal shortening velocities compared with those of the fast-twitch fibre types (Thompson, 2002).

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Classically, skeletal muscle fibres are identified because of their histochemically determined myosin ATPase activity as type I, IIa or IIb. Slow-fibre-dominant musculature, such as soleus, transversus abdominis and lumbar multifidus, contain primarily type I fibres, whereas extensor digitorum longus, gastrocnemius and vastus lateralis contain primarily a mixture of fast type IIa or type IIb fibres. Information regarding skeletal muscle adaptation to decreased loading/inactivity is derived from varied sources of investigation such as complete limb immobilisation models, limb unloading animal models and space flight. In both animals and humans muscle wasting is associated with selective loss and atrophy of specific muscles and of specific fibre-types (Oganov et al., 1980; Ohira et al., 1992; Edgerton et al., 1995; Alley & Thompson, 1997; Sandmann et al., 1998; Thompson et al., 1998; Widrick et al., 1999). Antigravity, predominantly slow-twitch type 1 fibre muscle, such as soleus, atrophies more than primarily fast-twitch type II muscles and extensors are more affected than flexors. This atrophic response occurs rapidly, with a reduction in soleus mass of up to 37% after 4–7 days of inactivity (Desplanches et al., 1990; Jiang et al., 1993; Caiozzo et al., 1994; Alley & Thompson, 1997; Sandmann et al., 1998; Thompson et al., 1998). Inactivity also induces a fibre-type transformation within specific muscles. Within a relatively short period of inactivity, the number of type 1 fibres in the antigravity muscles decreases, whereas the number of fibres containing fast-type myosin increases. After 7 days of inactivity the soleus and adductor longus muscles have an increased percentage of dark ATPase (fast) fibres – 11 and 26% respectively (Martin et al., 1989). In contrast, 7 days of inactivity has no effect on the percentage fibre-type distribution in the fast plantaris and superficial region of the medial gastrocnemius (extensor muscles), or the fast extensor digitorum longus. Importantly, these changes in muscle fibre-type composition impact upon the contractile functions of the muscles and the underlying mechanism responsible for the change in fibre-type composition is probably due to removal of the weight-bearing stimulus. Myofibril degradation in the early stages of atrophy can be attributed almost entirely to the reduced synthesis of protein. After the initial few days of inactivity the synthesis rate remains steady, whereas the degradation rates show a large increase, thus the majority of the protein loss after 3 days of inactivity can be attributed to the increased degradation rate (Baldwin et al., 1990). These findings suggest that both protein synthesis and degradation rates are altered with inactivity and play a role in skeletal muscle atrophy. The consistent feature of inactivity is limb muscle atrophy and the

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loss of peak force and power. Differences exist in the rate and mechanisms of muscle wasting and in the susceptibility of a given fibre-type to atrophy. Whilst these data are derived from both experimental animal and human studies undergoing space flight or bed rest, it is reasonable to argue that they may not fully replicate the situation in patients with neurological disease. However, given that the majority of these patients may have been on bed rest and have impaired ability to resist gravity, reduced exercise tolerance and certain conditions that constitute a relatively older age profile, it is likely that this information bears some relevance. In the clinical situation one rarely has the luxury of biochemical or histological profiles regarding muscle characteristics and clinical decisions regarding muscle loading and movement capacity must be judged on an empirical basis in the knowledge of pathophysiological processes.

ASSESSMENT OF MUSCLE IMBALANCE Muscle imbalance assessment is concerned with evaluating the capacity of the musculoskeletal system to execute the motor commands of the CNS. Aspects of function should include assessment of: ● ● ● ● ●

postural alignment muscle length muscle strength muscle endurance movement patterns.

Postural alignment Evaluation of postural alignment allows the clinician to generate hypotheses regarding resting muscle length and the likely implications upon movement patterns. It must be emphasised that at this point they are simply clinical hypotheses which must be confirmed or refuted by the appropriate clinical tests. Classic postural alignment has been described by Kendall et al. (1993), and variants of this alignment have also been described largely in relation to orthopaedic dysfunction. These variants are outlined in Figure 30.3. In patients with neurological damage, the spectrum of presentation is so variable that assessing posture in an upright stance position relative to a plumbline is often not practical. In these situations, a seated assessment may be necessary and localised assessment of posture, e.g. head/neck alignment or scapulothoracic alignment, may be an appropriate objective. Figure 30.4 outlines a classic postural alignment in a hemiparietic patient. Evidence of trunk or lower limb malalignment can also be obtained in supine lying, from which the therapist can determine the primary

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(A)

(B)

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(C)

Figure 30.3 Optimal postural alignment in orthopaedic evaluation indicative of minimal muscle activity and joint stress. (A) Kypholordotic pressure; (A) flat-back posture; (C) sway-back posture. (Adapted from Bryden & Fitzgerald (2001), with permission.)

areas of malalignment and the intervention necessary to address these discrepancies.

Muscle length A preliminary evaluation of muscle length can be determined by attempting passively to realign the deviant segments. This may involve attempting to realign a scapula that has become protracted and elevated (Fig. 30.5), or facilitating trunk extension in a patient who has adopted a flexed posture. If the therapist can facilitate a more efficient alignment by these relatively simple measures, then the direction of therapy must be to try to facilitate activity in the muscles which will provide the necessary mechanical realignment. If the therapist is unable to achieve efficient alignment through facilitation, then mechanical/ hypertonicity issues potentially restricting movement must be explored. Specific muscle length tests can be performed based on a knowledge of functional anatomy and

well-described muscle length tests (Janda, 1978; Kendall et al., 1993). In the hypertonic patient, one of the greatest clinical challenges is to determine whether muscle length changes are a consequence of mechanical adaptations within the connective tissue or of increased activity in the relevant muscle. Very often these are coexisting phenomena and the therapist may need to employ inhibitory techniques or positions prior to assessing muscle length with more formal tests. Therapists must also consider the possibility of articular restriction as a feature limiting movement, which must be evaluated and treated. The procedures for evaluating joint restriction are beyond the scope of this text but have been outlined in other sources (Maitland, 1986; Fitzgerald, 1992).

Muscle strength As previously discussed, absolute strength is of limited relevance in relation to functional tasks and activities of daily living. It is therefore more appropriate to

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(A)

(B)

Figure 30.4 Typical hemiparetic postural alignment of a high-level, ambulant subject. (A) Anterior perspective of a left-sided hemiparesis. The left arm is internally rotated and abducted (note the distance between the arm and side of trunk and the orientation of the cubital fossa). The shoulder girdle appears relatively good in this view, with trunk side flexion producing the apparent alignment difference. (B) Posterior view of the same subject. The left arm abduction/internal rotation is more visible here. Note that the point of the left shoulder is lower (due to trunk side flexion) but the contour of the shoulder appears elevated and protracted. This illustrates the importance of determining the position of bony landmarks in order to evaluate the dominant muscle synergies.

Figure 30.5 Preliminary realignment of scapula with therapist facilitation.

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determine the force required to move limbs and trunk rather than that required to move external resistance, as indicated in the DeLorme philosophies and general muscle hypertrophy training programmes. The level of loading applied is determined by the anatomical location. Lower-limb musculature needs to have adequate strength to tolerate body weight in varying combinations of trunk and leg position. Trunk musculature must be sufficient to maintain trunk stability, whilst allowing independent limb movement. The commonly observed clinical phenomenon in neurologically impaired patients is the inability to move limb and body segments independently because of lack of specific muscle control or more generalised muscle hyperactivity to maintain functional stability. A wide combination of strengthening techniques is available when using a functional approach and has been well reviewed by Davies (1994), Edwards (2002) and in Chapter 29. A key aspect of strength training is to provide adequate training stimulus, which will produce

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physiological adaptation towards achieving a functional goal and minimise the risk of overload, which may stimulate altered patterns of muscle synergy.

Holding capacity (endurance) The ability of antigravity muscles (postural muscles in the traditional sense and stability synergists) to maintain low-force isometric contractions is vital to their functional requirements. This ability can be tested in the usual muscle-testing positions in the middle or inner range, by asking the subject to hold the contraction. It is not the total time of static hold that is of interest, but the length of time the contraction is held without jerky (phasic) movements occurring (Richardson, 1992). For example, the trunk-stabilising muscles need to provide sustained contraction to stabilise the torso allowing limb motion. This can be assessed by asking a seated patient to lift a leg into flexion, thereby creating forces tending to displace the body. If this can be counteracted using muscle control, then the therapist can grade the stability endurance.

Movement patterns Muscle imbalance leads to abnormal movement patterns in which a functional activity may be achieved and be apparently normal but compensatory strategies and ‘trick movements’ may have been used (Jull & Janda, 1987; Kendall et al., 1993). Analysis of functional movement patterns is necessary to detect these abnormalities so that treatment can be planned for their correction. For example, a patient may use excessive spinal extension to achieve a functional goal of elevating the arm overhead. This is commonly seen as a substitution when there is an impairment of upper-limb function. Similarly, a patient with limited trunk control may use mass muscle activation in order to achieve a sense of stability. This often leads to compromised upper-limb function (as it is being used to provide fixation as opposed to prehensile tasks) or gross gait disturbance as dissociated trunk and limb motion is compromised.

CORRECTION OF MUSCLE IMBALANCE The essential criterion in attempting to correct movement impairment in the musculoskeletal system is to identify the underlying cause. Movement patterns may be altered as a consequence of mechanical restriction in one or more elements involved with the movement pattern. Careful testing can elucidate if these mechanical restrictions reside in the joints or the periarticular tissues and help to select the appropriate treatment techniques. Movement patterns that are deviant from optimal but are not associated with specific mechanical restrictions

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can be considered as a consequence of alteration in specific muscle co-ordination. This may be due to a lack of appropriate strength for the functional task (e.g. the ability of the lower-limb muscles to control body weight), overrecruitment of dominant/hyperactive muscles in the movement synergy or inadequate activation on the relevant synergic stabilising musculature. These are important aspects of movement impairment for the clinician to quantify because they directly dictate the direction of therapeutic intervention. The conventional hierarchy of exercise progression is to achieve isolated contraction in low-load situations of individual target muscles (Shumway-Cook & Woolacott, 1995). Following the acquisition of this level of skill, the therapeutic progressions are to increase the level of load and the complexity of the movement pattern to involve greater combinations of synergic stability and mobility demands. The majority of research regarding treatment protocols has been specific to musculoskeletal disorders in non-neurologically impaired patients. Whilst this body of data has shown validity in these aspects of rehabilitation, it has not yet been determined to be efficacious in neurological conditions. However, it must be acknowledged that it has been used routinely in many clinical centres worldwide but has yet to be exposed to the rigours of scientific scrutiny. Sahrmann (1987) gave an example of muscle imbalance syndrome in hemiplegia involving tightness of the iliotibial band. The typical hemiplegic limb position of abduction and medial rotation with knee extension reciprocates shortening of the iliotibial band. Adaptive changes within the upper limb have already been described earlier in this chapter and some graphic illustrations will follow in the case history below. The use of cycle ergometry and EMG biofeedback was proposed for correction of muscle imbalance in the stroke patients (Brown & DeBacher, 1987). Treatment involved retraining the activation of antagonistic muscle groups of the hemiplegic limb, as well as reciprocal exercise with some symmetry between the two limbs. Unloaded treadmill walking has also been utilised therapeutically in a variety of neurological conditions, such as partial and complete spinal cord injury, as well as stroke (Dietz et al., 1997; Liston et al., 2000; Kendrick et al., 2001). A number of conclusions can be drawn from these studies: 1. Spinal locomotor centres can be activated in paraplegic patients. 2. Increased leg extensor EMG is related to greater weight-bearing function and the ability to tolerate increasing load. 3. Successive reloading of the body is seen as a stimulus for extensor load receptors.

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4. The speed requires adjustment to the optimal rhythm in order to facilitate minimal assistance during the movement pattern. 5. The pelvis may need to be fixed to avoid deviation (lateral/posterior) so that limb loading occurs in a physiological manner. 6. In stroke there is a decrease in premature activity in plantarflexion caused by calf activation in terminal swing. 7. Following training, timing and structure of patterns of leg activity were similar to those seen in healthy subjects (Mulholland, 2002).

Retraining muscle activation Muscle activation patterns could be altered by increasing tonic input to the stability synergists or by reducing tonic input to the movement synergists. Richardson (1992) explained that the former method was thought to be more effective clinically and described strategies for retraining tonic activity. The first step is to isolate the stability synergist so that the movement synergist is not contracting. Tonic activity to re-educate slow-twitch muscle fibre function can be achieved by voluntary exercise or electrical stimulation. Richardson (1992) suggested voluntary activity involving low-force (20–30% of maximum voluntary contraction), sustained contractions of about 10 s each. Presumably rest periods, numbers of repetitions and frequency of exercise have yet to be researched but would also depend on the individual. Lowfrequency electrical stimulation can be used to change the muscle fibre properties but care must be taken as this can weaken muscle, and further research is required to establish appropriate frequency patterns (see Ch. 23).

Restoration of muscle length Techniques for restoring muscle length were described by Kendall et al. (1993). Briefly, shortened muscles can be lengthened using standard manual stretching or proprioceptive neuromuscular facilitation (PNF) techniques (see Ch. 23). A recent study has challenged this accepted approach to managing contractures using stretching (Shortland et al., 2002; see also Ch. 29). The investigators concluded that contracture of pennate muscles was due to loss of muscle fibre diameter, causing shortening of the aponeuroses. They therefore suggested that strengthening exercises would prevent or restore muscle length, but evidence to support this suggestion is required. Lengthened muscles can be shortened by exercising them using low-load contractions held for about 10 s in the shortened, inner range or by splinting them in this position (Kendall et al., 1993).

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Norris (1995a) discussed the problems of muscle imbalance around the lumbar spine and techniques for correcting length changes in specific muscle groups.

Restoring stability The functional interaction between synergists is restored by gradually increasing loads and speed (Richardson, 1992). Exercise programmes have been developed to improve the stability of the lumbar spine (Jull & Richardson, 1994; Norris, 1995b; Sahrmann, 2002). The principles of restoring stability fall into four stages, which were summarised by Norris (1995b) and involve: re-education of stabilising muscles; exercise progressions for static stabilisation; exercise progressions for dynamic stabilisation; and occupational or activity-specific stabilisation. Jull & Richardson (1994) described the use of feedback devices to aid in the isolation of specific muscles for assessment and retraining purposes.

CONCLUSIONS The potential impact of the muscle imbalance concept for improving the effectiveness of physiotherapy appears to be substantial but its future depends on research to establish its place in clinical practice. Collaborative research between physiotherapists, physiologists and biomechanical engineers should prove fruitful in elucidating the theory, producing guidelines for assessment and treatment and providing evidence of the effectiveness of corrective techniques. Neurological physiotherapists need to take part in research in this area so that application of the concept to neurological patients is applied and evaluated appropriately.

CASE HISTORY MQ was a 58-year-old man who suffered a left hemiparesis 1 year ago following surgery for removal of a brain tumour. His main difficulties were as follows: 1. severely painful left shoulder 2. gross limitation of left shoulder movement 3. impaired functional use of the left arm, as a consequence of shoulder girdle dysfunction, despite good disassociated motion in wrist, forehand and fingers 4. instability in standing due to poor alignment of the left lower limb, as a consequence of extensor spasticity

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5. compromised gait pattern due to extensor spasticity in the stance phase using knee hyperextension, internal rotation and abduction under load 6. no active ankle motion, with extensor spasticity dominant in weight-bearing.

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control with the addition of arm motion. This needed to be facilitated by the therapist until adequate strength and control were achieved (Fig. 30.8).

The treatment approach for the left shoulder involved a combination of graded joint mobilisations, initially in neutral positions and then progressing through various degrees of flexion and abduction (Figs 30.6 and 30.7). These were small-amplitude movements short of pain and ensuring not to produce hypertonicity. Joint mobilisation was supplemented with soft-tissue mobilisation and massage to increase compliance of the congested connective tissue. With improvement in pain-free motion, initially in flexion and subsequently abduction, the progression was to achieve some degree of active control within the available range. The strategies used were first to facilitate active scapular positioning on the thoracic wall and then to progress to maintaining scapular

Figure 30.7 Inferior humeral glide in abduction (within patient tolerance) to facilitate arthrokinematics of shoulder abduction and counterimpingement.

Figure 30.6 Inferior humeral glide in flexion (within patient tolerance) to facilitate arthrokinematics of shoulder flexion. The humeral head should translate inferiorly during arm elevation to prevent impingement. This requires a prerequisite degree of capsular compliance.

Figure 30.8 Therapist facilitation of active flexion, preventing superior scapular migration, supporting the weight of the limb and stimulating proprioceptive input.

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