Contractures (reduced joint mobility) are due to loss of extensibility in soft tissues spanning joints, and are a common complication of spinal cord injury.1,2 One study found that spinal cord injured patients had, on average, seven contractures (SD=6.2) at between 6 and 7 weeks after injury.1 Contractures are undesirable for many reasons but primarily because they prevent the performance of motor tasks.1,3,4,5 For example, elbow flexion contractures make it difficult for tetraplegics with paralysis of triceps muscles to bear weight through the upper limbs, and hence attain independence with transfers.6,7,8 Contractures also create unsightly deformities and are thought to predispose patients to spasticity, pressure areas, sleep disturbances and pain.1,2,5,8,9,10,11,12
Mechanisms of contracture
Contractures are either neurally or non-neurally mediated.13 Neurally mediated contractures are due to spasticity (ie, involuntary reflex contraction of muscles)13,14,15,16,17 and are a common sequelae of upper motor neuron lesions.18 Spasticity is usually managed with medication.18 While some believe that stretching also induces functionally important and lasting reductions in spasticity, this is yet to be verified with good quality studies.
Non-neurally mediated contractures are due to structural adaptations of soft tissues (for reviews see Gossman et al,19 Akeson et al,20 and Herbert21,22). Animal studies23,24,25 indicate that such changes occur in response to prolonged immobilisation, particularly immobilisation of soft tissues in shortened positions. Ten days immobilisation of rabbit ankles in plantarflexed position (the shortened position of the plantarflexor muscles) results in approximately a 10% reduction in resting length of soleus muscle-tendon units,25 which is sufficient to produce functionally significant loss of ankle joint mobility. Muscle shortening is associated with a decrease in the number of sarcomeres, changes in the alignment of intramuscular connective tissues and a decrease in tendon resting length.23,24,25,26,27,28,29,30,31,32,33,34
Effects of muscle stretching
Stretch has become a widely accepted means of treating and preventing contractures in people with spinal cord injuries.35,36,37 For instance, it is now accepted practice in spinal cord injury units for therapists to routinely administer between 2 and 5 min of stretch a day to each major group of soft tissues, particularly when patients are confined to bed immediately after injury. Consequently, it is not unusual for therapists to spend between 30 and 60 min a day with each patient, administering stretches. Despite the time, effort and resources devoted to administering stretches in this way, few rigorously designed studies have examined the effectiveness of this intervention.38
The use of stretch to treat and prevent contractures is usually justified by animal studies23,39 that indicate the deleterious structural and morphological changes associated with immobilisation in shortened positions can be prevented25 or reversed23 by prolonged immobilisation in lengthened positions (ie, continuous stretch). Continuous stretch of this kind appears to trigger remodelling of soft tissues. However, while animal studies show that continuous stretch can reverse deleterious length adaptations in muscles, the effect of shorter periods of stretch is less clear. Only two studies29,40 have investigated the effects of short periods of daily stretch on soft tissue extensibility. These studies found that when the soleus muscles of mice were immobilised at short lengths, deleterious length adaptations such as decreases in sarcomere number and muscle resting length could be partly prevented by interrupting the immobilisation with as little as 15 min of stretch each day. Thirty minutes of stretch was enough to completely prevent these changes. No study has yet examined the effect of less than 15 min daily stretch in an animal model, though stretches of this duration are typically applied in the clinic.
A large number of human studies have examined the effects of stretch on the extensibility of soft tissues. However, the majority of these studies have only examined the effects of stretch on joint mobility and range of motion within minutes of the cessation of the stretch intervention. Increases in joint mobility observed soon after the cessation of stretching are primarily due to viscous deformation,41,42,43,44,45,46,47 and need not reflect the structural adaptations of soft tissues required for lasting increases in extensibility.22 For this reason, studies which only report measurements taken within minutes of the removal of stretch cannot provide evidence about the effectiveness of particular types of muscle stretching for the treatment and prevention of contracture. Only studies that measure joint mobility many hours or days after the removal of stretch, when the transient effects of viscous deformation have subsided, can be validly used for this purpose.
To our knowledge only one randomised study38 has investigated lasting effects of stretch on contracture in people with spinal cord injury. This study examined the effect of 4 weeks of 30 min daily stretches (7.5 N.m) to the ankles of recently injured paraplegics and tetraplegics. Ankle mobility was measured 24 h and again 1 week after the removal of stretch. Despite excellent statistical power, no treatment effect was found. The authors speculated that this may have been because co-interventions (such as routine positioning of ankles at 90 degrees in wheelchairs) were sufficient to reverse or prevent plantarflexion contractures, and muscle stretching provided no additional benefit. Alternatively, it may have been that the stretch protocol was of insufficient intensity or duration. These findings differ from those of two well-designed randomised trials on other populations, both of which found a therapeutic effect with 4-24 h stretch a day in head-injured4 and elderly bedridden patients.48 However, the results of both these studies may reflect viscous deformation rather than lasting increases in tissue extensibility. Clearly, therefore, more randomised clinical trials are needed to determine if stretch is effective for the treatment and prevention of contractures, and if so, to clarify the optimal dosage of stretch.
Optimal stretch protocol: The challenge for therapists is to use the available evidence to make reasonable decisions about clinical practice. It is disconcerting that the first randomised clinical trial on stretching in spinal cord injured patients found no clinically worthwhile effect, despite the application of daily stretches well in excess of those typically used in clinical practice (ie, despite the application of 30 min of stretch per day). However, the rationale supporting the use of stretch is strong. Given the serious consequences of contractures, we do not recommend that therapists discontinue stretching on the basis of one negative randomised trial. Instead it is probably appropriate that therapists continue to provide stretches to spinal cord injured patients, at least until further randomised trials indicate otherwise. In the meantime, it may be prudent to apply stretches for as long as is practically possible (ie, for at least 20 min, and perhaps for as long as 12 h a day) in order to maximise the likelihood of attaining a therapeutically worthwhile effect.
If stretches are to be applied for more than a few minutes a day, therapists need to move away from the labour-intensive tradition of manually applying stretches with their hands. Instead, limbs should be positioned with at-risk soft tissues in stretched positions, and where possible positioning programs should be incorporated into patients' rehabilitation programs and daily lives. Often only relatively simple equipment is required for this purpose. For example, the hamstring muscles of patients confined to bed can be readily stretched for sustained periods of time with a splint and pulley device attached to the bed (Figure 1). The extrinsic finger flexor muscles of the hand can be stretched with a simple wooden device (Figure 2), and the shoulder extensor muscles of seated tetraplegics can be stretched by positioning the arms on high tables (Figure 3). Hand splints are also an effective way of positioning soft tissues in lengthened positions. A splint that immobilises the metacarpophalangeal (MCP) joints in flexion and interphalangeal (IP) joints in extension may help prevent MCP hyperextension and IP flexion contractures49 (both of which are common in tetraplegics with lesions at or above C5, particularly if oedema is also present). Stretches applied in any of these ways can be readily sustained and easily administered by therapists and carers. Of course care needs to be taken to ensure that strategies instigated to prevent contractures in one group of soft tissues does not promote contractures in the antagonistic group of soft tissues.
Preventing and anticipating contractures: It is widely believed that contractures can be more readily prevented than treated and that less stretch is required to maintain than increase the extensibility of soft tissues. Though the validity of these beliefs has not yet been substantiated, therapists are well advised to concentrate efforts on preventing contractures. For example, supination contractures of the forearm (a common contracture of tetraplegics with C5 lesions) may be prevented by ensuring patients spend equal lengths of time each day sitting with forearms pronated and supinated. Minor modifications to the arm rests of wheelchairs may be required, but otherwise this is a relatively simple positioning protocol to implement. In contrast, once supination contractures are established it is difficult to effectively stretch the forearm, and often cumbersome splints are required.50 In the same way, hip and shoulder adductor contractures may be prevented in patients confined to bed by simply positioning patients for at least some of each day with shoulders2 and legs abducted rather than adducted.
Factors that predispose patients to contractures: The skill of preventing contractures largely lies in accurately predicting them.51 At-risk soft tissues are those habitually held in shortened positions. Fortunately, it is possible to predict soft tissues likely to be held at short lengths by looking at factors such as the pattern of innervation, pain, oedema, independence with various activities of daily living (ADL), and the position in which the patient spends the majority of each day (ie, in bed or in a wheelchair; see Table 1). For example, patients with complete C5 and C6 tetraplegia are susceptible to elbow flexion contractures. These patients have paralysis of the triceps but not biceps muscles. Consequently, they tend to sit and lie with their elbows flexed. The problem is particularly apparent in patients nursed in a supine position for extended periods of time. From this position it is difficult for patients with paralysis of the triceps muscles to passively extend their elbows once flexed.
Pain increases susceptibility to contracture because it increases the tendency to contract non-paralysed muscles, which in turn increases the time soft tissues spend in shortened positions. Independence with activities of daily living also helps predict susceptibility to particular types of contactures. For instance, C6 tetraplegics who transfer independently throughout the day, passively extend their elbows while bearing weight through their upper limbs6,7,8 and are therefore less likely to develop elbow flexion contractures than more dependent C5 or C6 tetraplegics.
The pattern and extent of spasticity will also influence susceptibility to contracture.18 This is not only because spasticity directly influences the extensibility of muscles (ie, contributes to neurally-mediated contractures, as discussed above) but also because spasticity increases the time that muscles and surrounding soft tissues spend in shortened positions.13,16,52,53 For example, constant spasticity of elbow flexor muscles may increase the amount of time the elbow remains in a flexed posture, and hence initiate structural adaptations of the soft tissues spanning the flexor aspect of the elbow. However, just as spasticity can indirectly contribute to contracture, so too can it prevent it. Patients otherwise susceptible to elbow flexion contractures can benefit from regular and strong elbow extensor spasticity (this pattern of spasticity is more common in C5 than C6 tetraplegics), because the spasticity can act to minimise the length of time the elbow spends in a flexed position.
Implications of contractures for individuals with spinal cord injuries: The implications of slight losses of extensibility in soft tissues varies with level of motor function (see Table 1). Thus, while most contractures are undesirable, the prevention of some is more important than others. Slight loss of extensibility in the soft tissues spanning the flexor aspect of the elbow will have few functional implications for C5 tetraplegics unable to bear weight through the upper limbs. However, the same loss can prevent C6 tetraplegics from attaining independence with transfers.6,7,8 In the same way, slight loss of extensibility in soft tissues spanning the plantar aspect of the ankle (eg, the soleus muscle) will have little functional implication for a high-level wheelchair-dependent tetraplegic but marked implications for a walking low-level paraplegic. Clearly, concentrated effort should be directed at preventing loss of extensibility where such loss will impose important functional limitations.
Excessive tissue extensibility can hinder function: Sometimes excessive extensibility is just as undesirable as limited extensibility and can prevent patients from performing important functional tasks. Excessive extensibility in the hamstring muscles can prevent C6 tetraplegics from sitting unsupported on a bed with knees extended,37 a skill important for independent dressing and transferring. Provided the hamstring muscles are not excessively extensible, the passive length of the hamstring muscles prevents the patient falling forwards into full hip flexion37 (Figure 4a). However, the hamstring muscles can not prevent the body falling forward if they are too extensible (Figure 4c). Therefore patients with excessive hamstring extensibility are disadvantaged because they must rely on their upper limbs to support their body. On the other hand, limited hamstring extensibility will prevent the patient from positioning the center of mass anterior to the hips, causing the body to fall backwards (Figure 4b). In this instance at least, there is a fine line between sufficient and excessive extensibility, and some patients may benefit from strategies that promote, rather than prevent, loss of extensibility.
Limited tissue extensibility sometimes assists function: In unique circumstances, contractures can assist functional movement. An effective passive tenodesis grip in C6 and C7 tetraplegics depends on contractures in the flexor pollicis longus and extrinsic finger flexor muscles.54,55,56,57,58 Contractures in these muscles ensure that active wrist extension passively pulls the fingers and thumb into flexion. In this way, objects can be passively held between the thumb and index finger or in the palm of the hand. The challenge for therapists is to instigate appropriate interventions that promote loss of extensibility in the extrinsic finger and thumb flexor muscles while avoiding contractures in the joints of the hand.54