Causes of deformities and aims of therapy and management

Some of these causes are interwoven and their relationships are discussed.

Immobility

General immobility is associated with persistent posture and very few, if any, movements in a child. The causes may be due to:

Physical impairment of hypotonicity, hypertonicity, weakness with limited ranges of motion, a few abnormal, inefficient movement patterns, impaired postural control with prolonged abnormal postures. The combination of dystonia and spastic hypertonia causes more severe immobility.

Other causes such as sensory loss (mainly blindness), severe perceptual-motor defects, especially those related to space and body image, emotional problems, especially if the child is fearful or withdrawn, severe intellectual impairment, social deprivation and malnutrition. Most of these reasons tend to create lethargic, unmotivated children, who prefer to be immobile.

When many of the above causes of immobility combine in the same child, deformities are most likely to occur. Therefore, immobile children who have severe multiple disabilities are particularly prone to their deformities becoming contractures.

Partial or even very minor immobility of children compared to their able-bodied peers happen in mild-to-moderate disability. Some of the more severely involved children can acquire a few abnormal postures and stereotyped movements for partial mobility.

Aims. Therapy, special equipment including or-thoses and adapted environments aim to enable children to become more mobile. The degree of mobility depends on the severity of the condition. The aim is to use interesting playful activities to motivate actions and as much appropriate mobility as possible throughout the day.

Hypotonicity

The floppy baby or very young child with hypotonia may be due to many neurological causes other than cerebral palsy. Hypotonic babies or very young children with cerebral palsy may become hypertonic, dyskinetic or ataxic as they develop. They are initially immobile and may sometimes be left lying for long periods in one or two positions, which can create deformities. For example, the frog position of the legs in prone, supine or with the child propped up on pillows in the half-slumped sitting position may all lead to deformities especially in the spine and hips. Anterior subluxation or dislocation of hips may be found in such cases.

A common characteristic of most floppy babies is the absence of all or some of the normal postural mechanisms. The neck, trunk, shoulder and pelvic girdle muscles are not being activated by these mechanisms, and are weak and hypotonic. Hypotonia is not always associated with total weakness. Fair, though weak, voluntary movement may be present, but it is not enough to make the child mobile. Without the presence of postural mechanisms a child cannot get out of his few positions during the day and night. Postural control is therefore absent or poor, preventing reliable function.

The baby with ataxic cerebral palsy has hyper-mobile joints and may later develop some postural mechanisms being able to sit, stand and walk unsteadily and with a delayed development. There are common abnormal deformities such as sitting with legs in frog position and round backs; standing with round backs, lordosis, hyperextended knees (back knees, recurvatum), valgus knees (knock knees), varus knees (bow knees) and pronated feet (flat feet). Children who develop spasticity retain trunk hypotonia with stiff limbs. Children who become dyskinetic retain hypotonic trunks with fluctuating tone, in trunk and/or limbs. They have similar deformities as in ataxia due to a variety of causes (see sections ‘Spastic cerebral palsy’, ‘Dyskinetic/dystonic cerebral palsy’ and ‘Ataxic cerebral palsy’ in Chapter 1).

Aims. Train postural control, strengthen and correct abnormal postures with equipment where necessary.

Hypertonicity

Historically, spasticity was considered the most important cause of deformity. Currently there is still a focus on ‘spasticity’ by some physiotherapists and also in many studies on the use of botulinum toxin A (BTX A), usually with physiotherapy. There are different types of hypertonicity and spasticity needs clarification, as spasticity can need therapy for stiffness, weakness or incoordination of muscle activations (see below). Focus on spasticity includes the use of baclofen (Albright & Neville 2000; Lin 2004) and neurosurgical selective dorsal rhizotomy (Peacock & Staudt 1991; McLaughlin et al. 1998).

Types of hypertonicity. The dystonic-dyskinesia type of cerebral palsy is less liable to have deformities owing to fluctuating tone. There is a persistent type of dystonia together with spasticity, as well as a specific rigidity type in post-traumatic cerebral palsy, which do cause deformities. In these children a lead-pipe rigidity is felt on stretching throughout their joint ranges. Many workers focus on deformities in the spastic type as it is the commonest type of cerebral palsy and most liable to progressive deformities. In the spastic type, there is an abnormal reaction to rapid stretch (a velocity-dependent hyperactive stretch reflex), described by neurophysiol-ogists, and also called a clasp-knife spastic reaction. This physiological test of spasticity is not associated with abnormal posture which causes deformities (Lin 2004).

The creation of the deformities is, however, dependent on the neurological and orthopaedic (musculo-skeletal) views. Deformities are associated with immobility in habitual abnormal positions, stiffness (Brown 1985), muscle shortening and muscles overlengthening. There are other important aspects that need consideration, such as the recognition of aspects of abnormally coordinated movements (abnormal synergies), weakness and inefficient muscle work, and especially in compensation for absent or atypical postural mechanisms. These causes together with growth and biomechanics are discussed below.

There is a tendency for spastic muscles to shorten, which will cause one aspect of the deformity (Tardieu et al. 1982; Dietz & Berger 1983; Huf-schmidt & Mauritz 1985; Cosgrove 2000). Shortening hypertonic (‘hypoextensible’) muscles pull the joints into abnormal motor patterns involving the whole child or at least of the whole limb. Shortland et al. (2002) and Fry et al. (2004) have used ultrasound to study muscles in spastic cerebral palsy, and one finding was that weakness of muscles may contribute to muscle shortening and atrophy. They have included research on muscle length in these children. Akeson et al. (1987) consider that muscle contracture is related to length changes whereas stiffening of joints is more related to movement deprivation. At first ‘hypoextensible’ muscles with or without hypertonic stiffness can be overcome in a young child but later it can become fixed. Although one joint with its muscles may be more deformed than the others within a motor pattern, it is important to check each joint as well as observe the pattern of abnormal posture and movement.

Muscle imbalance. There is a common assumption that spastic muscle is strong with a weak antagonist (Bobath & Bobath 1984; Reimers 1990). This is called a muscle imbalance, which is assumed to lead to deformity. Although some orthopaedic workers still talk of the muscle imbalance, they unfortunately say that the spastic muscles are strong and the antagonists are weak. This is rarely so. It is the strong pull of the short spastic muscle that is strong, and not the spastic muscle work itself. Once spasticity is decreased, spastic muscles often reveal weakness. The antagonists of the spastic muscle groups are working at a mechanical disadvantage to the tight pull of the stiff, short spastic muscle groups. Therefore, the antagonists cannot shorten to stretch the spastic agonists. As antagonists cannot counter the pull of the spastic muscles, they appear too weak to do so. In time they really become weak from disuse and inability to be active through their full ranges. It is necessary to prevent deformity by mobilising and lengthening the spastic muscles and strengthening them and their antagonists. As full a range as possible is needed for all muscles.

Ross and Engsberg (2002, 2007) have investigated the relationship between spasticity and strength and also found that there was no ‘muscle imbalance’ at a joint. They also found that the degree of spasticity (velocity-dependent resistance to passive stretch) had no relation to the amount of strength in that muscle. They consider that ‘muscle weakness, and not spasticity may be a prevailing impairment’ in cerebral palsy and that their research on the individuals with spastic diplegia showed more involvement distally than proximally in the legs. There was little to no significance of spasticity with function, but strength was correlated with a number of specific variables in functional measures.

The impairment of weakness is further discussed in the next section.

Aims. The therapist and especially those involved in daily care aim to carry out correct management of the abnormal postures and abnormal movements which appear in function as a priority, as well as maintain the elongation of short muscles and soft tissues in selected orthoses and equipment. Encourage a variety of active postures and movements in daily motor functions. See aims for strengthening below.

Weakness – general and specific

Aims. Considering the discussion points above, the clinician aims to strengthen spastic muscles and their antagonists in as full a range as possible and improve bilateral strength in asymmetrical distribution of weakness. Postural mechanisms need to be developed in active motor activities for the whole child to avoid both specific and general weakness. Developing fitness in leisure activities includes strengthening.

Abnormal co-contraction and abnormal synergies

The abnormal postural mechanisms or their absence lead to abnormal postures against gravity. The normal postural mechanisms are discussed in Chapter 5. In Chapter 9, there are practical therapeutic suggestions for assessment and activation of postural mechanisms within all developmental functions. Compensations result from absent or poor postural mechanisms and may activate excessive co-contraction to maintain balance. The legs appear to be stiff and straight similar to the positive supporting action seen in normal infants. There can be compensations which use a variety of abnormal postures for balance such as those mentioned above in hypotonic ataxia and the examples in Chapter 9 in all antigravity postures.

The abnormal postures are also combined with abnormal movement synergies, which include co-activation (co-contraction) and abnormal recruitment patterns (Tedroff et al. 2006). These abnormalities are not due to hypertonicity but due to motor control problems (Shumway-Cook & Wool-lacott 2001). The postural co-contractions and co-activation in movements are also seen in early normal development or early stages of learning a new motor skill. They do not necessarily create deformities but the persistence of co-contraction in cerebral palsy can lead to limitation of range of the muscles.

There are also abnormal synergies with the difficulties in isolated muscle action seen in lack of selective motor control. For example, a child with spasticity cannot easily dorsiflex an ankle without also flexing hip and knee. Muscles for grasp may not be activated without flexion of wrist and elbow. If a particular movement pattern is used repeatedly for daily functions, then this may cause deformity. In some individuals, persistence of such movement patterns in individuals has also been related to abnormal reflex patterns discussed in the next section.

Aims. Provide a variety in motor patterns within active developmental functions and active exercises, as well as improvement with specific treatments. Develop postural mechanisms within developmental functions.

Abnormal reflex activity (see Table 8.3)

These activities may be used by individuals with dyskinesia or spasticity. There may be persisting infantile reflex patterns or pathological reflex reactions. It is not the reflex as such that lead to deformity but the recurring unwitting stimulation of these patterns by those handling a person with cerebral palsy. Children or older people may only be able to move by repeatedly using reflex patterns as the only resource available to them. They learn to activate specific abnormal reflex patterns in their efforts to function. This perpetuates the reflex patterns which lead to deformities. However, not all children depend on a strategy of moving by activating reflexes, and are not being dominated by any reflexes. Examples of reflex patterns are:

Asymmetrical tonic neck reaction (ATNR) may be used by turning the head to the side of a more useful arm for it to reach for a toy with reflex arm extension. A subsequent head turn away from this extended arm obtains a reflex flexion on the occipital side of the head. This arm flexion brings the toy to midline. Another example is of a child with asymmetry, walking with head to one side to stiffen reflex leg extension for stance and head turn away from the extended leg to allow it to bend for stepping. The persistent ATNR to one side creates asymmetrical limb postures by head turning which may lead to deformities in the limbs, a scoliosis and/or a torticollis. Extensor postures are associated with ATNRs, so head flexion in midline enables limitation of the ATNR. In some cases, ‘windswept’ legs which are associated with persistent ATNR to one side can later lead to hip subluxation due to the flexion-adduction on the occipital side. This abnormal positioning is combined with the effect of gravity.

Symmetrical tonic neck reflexes is rare but may occur in some very severe cases. Immobility and lack of treatment may lead to deformities within these patterns, or in remnants of them.

Reflex stepping may aggravate hypertonic plantar flexors, adductors and extensors if this reflex is used to ‘walk’ the child frequently. However, the flexion phase of stepping can modify the pattern although the equinus of the ankles, reinforced by reflex stepping, may persist.

Excessive supporting reaction or antigravity reflex may be overstimulated by, say, baby bouncers or inappropriate walkers and increases the deformities of the legs, especially equinus and extensor-adductor postures.

Active use of total flexion reactions, withdrawal reflexes in kicking, during rolling, crawling, kneeling. The withdrawal reaction which repeatedly combines hip–knee and ankle flexion rather than a variety of synergies including the hip flexion, knee extension and ankle flexion needed for future walking. The repeated use of flexion in all these movements or postures tends to flexion deformity.

Use of total extension reactions as in using the extensor thrust in active kicking, when bounced on the feet in standing, in order to achieve rolling and creeping with abdomen on the floor, may lead to deformities into these patterns of extension.

Aims. When reflex reactions persist in some children, use methods to modify them. As suggested in earlier chapters, the specific methods for development of motor functions will spontaneously decrease or overcome early reflexes. Train a variety of functional motor patterns so that infantile patterns of reflexes need not be used.

Asymmetry

See abnormal postural asymmetry in prone, supine, sitting, standing and walking development (Chapter 9). Deformity may be due to:

Aims. Correct excessive asymmetry. Develop normal symmetrical and asymmetrical motor functions. Use raise on shoes to adjust unequal growth of lower limbs. Check raise by placing different thicknesses of small books under the shorter foot to establish when pelvic adjustment takes place with bilateral weight bearing.

Involuntary movement in one repetitive pattern

Any repeated flexor spasms or involuntary dysk-inetic kicking with hip and/or knee flexion, or a flexor involuntary repeated pawing of a leg, may give rise to tightness in the knee or hip. Miller (2007) reports loss of standing for transfers due to knee flexor deformity in young adults or adolescents with athetosis (dyskinesia) combined with spasticity. Similarly and less commonly, children have repetitive extensor spasms or rotary involuntary movements, which may create tightness. Older people with dyskinesia may use muscle tension to control involuntary movements which result in tense abnormal postures with muscle pain.

Aims. Reduce tightness. Treat pain.

Growth factors

There are four main factors which cause or aggravate the development of deformity:

Aims. Monitor posture and movement throughout the lifespan of a person with cerebral palsy. Treat when indicated, particularly during growth spurts. Therapy needs to increase activity and take care to include stretching of limbs and trunk.

Biomechanics (see sections ‘Abnormal postures in standing’ and ‘Abnormal gaits’ in Chapter 9)

The biomechanics related to deformities are as follows:

These abnormal postures, if uncorrected, can further disturb balance due to increasing abnormal alignment with growth. Green et al. (1995) have observed abnormal biomechanics in lying, sitting and standing. Butler and Major (1992) and Farmer et al. (1999) have observed biomechanics in upright postures. Gage (1991, 2009) discusses biomechanical problems in gait analyses.

Biomechanics of limb movements are affected by moving in relation to gravity.

Aims. Improve postural mechanisms particularly stability and counterpoising of limb motion. Improve postural alignments and weight bearing both actively, with orthoses and equipment. Apply the biomechanics for movements and strengthening involving use of gravity for assistance, eliminating gravity for neutral actions and increasing muscle actions against gravity for strength (see Chapter 9).

Deformities and gait

Gait analyses for conservative therapy without surgery are discussed in Chapter 8. See Figs 9.164–9.170 for gaits and therapy suggestions.

Upper limbs. The aims of BTX A injections or orthopaedic surgery are for function of hands, cosme-sis and hygiene (Cosgrove 2000; Graham 2004; Horstmann & Bleck 2007).

Orthopaedic surgery. Procedures are for wrist flexors, or stabilisation of the wrist joint, lengthening of pronator teres or other muscles. Occupational therapy is used in either the follow-up of surgery or in prevention of deformity and development of function. There is an overlap of occupational therapy with physiotherapy. Arm deformities and function are discussed in this chapter as well as in Chapters 9 and 10.

Spastic hemiplegia

The upper limb deformities are shoulder girdle protraction, shoulder flexion, adduction and internal rotation. A few may develop subluxation or dislocation of the gleno-humeral joint. There is tightness of the pectoralis major and subscapularis. There is elbow flexion with pronation. The tight flexors and pronators together with very weak supinators are present and may occasionally lead to sublux-ation of the radial head. The wrist and fingers are flexed with thumb flexed, adducted in the palm. The metacarpo-phalangeal joint may be a secondary deformity in the thumb. Wrist ulnar deviation rather than radial is more common. In individual gaits, a hemiplegic arm may also be retracted and hang down straight with elbow pronated and does not swing or be held in the arm position above without swing. A very young child or one with mild-to-moderate involvement will only show the flexed arm pattern on running or jumping. Early therapy usually prevents the arm from becoming more severe.

The lower limb usually begins with a dynamic plantarflexion deformity, which becomes an equi-nus contracture together with a smaller, shorter limb as the child grows. Equinus gait or ‘toe-stepping’ may at first have a straight hip and knee with a minimal limp. Later if severity increases or in more severe cases, equinus is accompanied by hip–knee flexion with adduction–internal rotation of the affected leg. Compensation for the equinus may be a vaulting action to assist with clearance. Compensation for equinus on the affected side can also be hyperextension of the knee or use of valgus of the foot to obtain a plantigrade foot. Miller (2007) reports that some children with hemiplegia are ‘toe-stepping’ on both the hemiplegic side and the unaffected side to avoid a limp.

A gait in hemiplegia may have the affected side retracted with weight in front on the other leg. A momentary stance on the hemiplegic side only allows a short step with the other leg.

Gait is affected not only by weakness but also by inadequate length of plantar flexors in swing phase and stance phases. Below-knee plaster (casting) or orthosis has been used in the early stage. A hinged ankle-foot orthosis (AFO) with or without an injection of BTX A is used for the early dynamic phases. Casting together with BTX A may be another option. These procedures delay surgery until a child is well over 6 years. Depending on severity, surgery may be a lengthening of Achilles tendon (z-plasty) or gastrocnemius slide. In more severe cases there is co-contraction of short hamstrings with quadriceps and equinus, valgus, varus and foot problems. For the hip, knee and foot deformities there are various surgical procedures according to the severity of the hemiplegia (Graham 2004), which are followed by solid AFO or ground reaction AFO. However, many children with hemiplegia achieve walking without walking aids and following conservative physiotherapy. They may or may not develop fixed deformities later.

Spastic diplegia

Generally, the walking of children with diplegia is much slower than in able-bodied children, and their choice of velocity is most efficient but in later years their inefficient walk leads to fatigue (see subsection ‘Prognosis for walking’ in Chapter 9). Deformities may be mild, not interfering with walking, but if more severe may lead to deterioration of walking.

Upper limbs. There may be persistence of arms held up in the air in toddler ‘high or medium-guard’, or in a ‘tight-wire walking’ position as well as excessive arm saving reactions. In early independent walking, reciprocal arm swing is absent. Abnormal postures of both arms in the hemiplegic-flexed pattern are mentioned above.

Lower limbs. In the toe-stepping gait in young or mild diplegia, there is initially a toe walk in equinus with a normal or stiff knee extension and mild internal rotation of hips. Toe first and not the normal heel strike on initial contact following the leg swing is common. With arms in high guard a child can walk fast on toes and falls rather than stop. This is managed with ankle-foot orthoses and physiotherapy to gain balance and control. Walking with a plantigrade foot becomes possible in this case.

Knees may overflex on swing and on weight bearing. Hip and knee flexion may occur to allow a plan-tarflexed foot (or equinus) to swing and clear the ground, and once on the ground, hip and knee flexion occur to push the heel to the ground. However, as mentioned above, there may instead be equinus on initial foot contact with hip and knee straight. Lack of heel strike after swing may be compensated by flexion of hips with hyperextension of the knees to press the heels to the ground in pronation. This is usual with extensor patterns or excessive anti-gravity support as the forefoot strikes the ground. Hyperextended knees if untreated in middle childhood may cause much knee pain in adolescence and a wheel chair may later be needed (Miller 2007). Miller suggests a calf-length articulated AFO that limits plantarflexion to assist hamstring strengthening over time to counter the knee hyperextension. Hyperextension can be treated with operations for equinus if that is the cause.

A child may become stiffer with spasticity and the equinus and varus increase. In these cases, BTX A injection is used to tolerate the ankle-foot orthoses and physiotherapy continues together with passive stretching and strengthening exercises for feet and legs as well as balance training.

A diplegic gait that is more common is presented in the following pattern. There is hip flexion–adduction–internal rotation with knee flexion and equino-varus, or feet flat with valgus. In diplegia the hips may adduct and legs cross when the child is supported, and adduct, internally rotate and flex when the child is walking independently. A wider base of the feet is achieved with flexed closely adducted (valgus) knees as the child cannot balance on the small base created by adduction of the legs. Feet may also be in valgus to overcome equinus.

There may be a ‘jump gait’ of hip and knee flexion with equinus on initial foot contact followed by hip and knee extension during stance. This has a jumplike appearance. Graham (2004) may manage this gait with articulated orthoses. The equinus may be apparent and secondary to hip and knee flexion, so BTX A is not used for plantar flexors.

In the ‘crouch gait’ the ankle is excessively dor-siflexed with increased hip and knee flexion. These children may have been toe walkers with straight or mildly flexed hip and knees before becoming an adolescent with a crouch gait. BTX A and various surgical procedures are used by different surgeons. Ground reaction AFOs may be used in milder crouch gaits before surgery or following surgery. With increased severity the flexion contractures are seen together with bony torsion deformities and joint problems in hips, knees and feet due to the biomechanics of walking (Graham 2004). Damiano et al. (1995a) have markedly improved crouch gait with strengthening exercises against resistance for quadriceps and hip extensors. Presumably the deformities are then largely dynamic.

Various operations are recommended to overcome hip–knee flexion in crouch gait, such as hamstring and psoas lengthening and correction of bony deformities if present. Ground-reaction ankle-foot orthoses may follow some operations on muscles and soft tissues in less severe cases.

Surgery is suggested when there is increased knee flexion in both foot contact and mid-stance phases of gait, together with a markedly increased popliteal angle on physical examination. Surgery is usually used for fixed knee flexion deformity. Examples are partial hamstring tenotomy, hamstring slide, hamstring transplants, with various lengthening procedures and transfers of other muscles. Surgery to lengthen short hamstrings has been used when hamstrings create a kyphotic sitting posture in older people. Post-operative physiotherapy may include knee splints range of motion exercises, strengthening of both extensors and flexors of hips and knees. Treat the hamstrings for two-joint muscles. Rehabilitation teaches a child to move with his ‘new legs’ and work on extension. Weight bearing depends on the advice of the surgeon.

Many children with diplegia have asymmetry between the legs of individual weak muscle groups but pelvic asymmetry and scoliosis may not always be present. However, when scoliosis is present, it is due to unequal weight distribution and/or difference in leg length. There may be limited mobility in hips, pelvis and lumbar spine. Backward tilt of the pelvis with flat lumbar spine may be present in some children, or excessive forward pelvic tilt with lumbar lordosis. There may also be round backs (kyphosis) with lordosis and the hip flexion. Spasticity and deformity are more in the psoas, hamstrings, rectus femoris and gastrocnemius. Postural malalignments may be secondary to limb problems or persist from abnormal sitting postures and poor postural mechanisms against gravity.

The pelvis often rotates abnormally in all ‘spastic gaits’. The rotation may be backwards, so the leg appears retracted and behind the other. Usually the front, more able leg takes more weight. However, there may be the situation when a back leg may take more weight and allow the forward leg to step, take its momentary weight and then transfer on to the back leg, which only has time to take a small step and cannot get in front of the forward leg.

If the child takes a step, his stiffness may be so great that he has to lean back to push his leg forward. He has an antero-posterior jerky walk. Lateral ‘waddle’ is associated with spastic adductors and weak abductors. It is also involved with inability to stabilise the pelvis or to adjust the trunk when counterpoising in standing on one leg. The trunk and head may lean forward to help overcome stiff spastic extension or use much head and trunk mobility to counter the lower body stiffness to maintain balance (postural control). Orthopaedic surgical procedures are indicated for excessive hip extension with abnormal pelvic tilts (Sussman 1992; Horstmann & Bleck 2007).

If a child has an early gait which is efficient, this is frequently maintained until adulthood. If the child is struggling to walk and just managing with much flexion, then retaining walking is less likely. Weight gain and prolonged sitting will also decrease the future likelihood of walking with or without crutches, sticks and other aids.

Spastic tetraplegia (quadriplegia)

This type is usually more severe with weakness, loss of selective motor control, retention of infantile reflexes, muscle imbalance, abnormal posture and general spasticity. The whole body is much more involved than the other types of cerebral palsies. Deformities of limbs, position of pelvis and trunk, and abnormal weight transference are similar to spastic hemiplegia and spastic diplegia usually with greater asymmetry and severity. The leg deformities can be accompanied by unilateral or bilateral hip dislocation, pelvic obliquity and sco-liosis. As hip problems are frequently encountered, there is further discussion below in the subsection ‘Hip flexion–adduction–internal rotation’.

Bone density problems. In severe diplegia and tetraplegia, there are more bone density problems due to poor nutrition and some medications for epilepsy, and there is less likelihood of weight bearing and independent standing and walking. However, there are some who will continue to use a walker until 12–13 years (Miller 2007). Older children are encouraged to use standing frames and well-supported walkers to maintain weight bearing for transfers, general fitness and possibly for bone density problems. In early childhood, standing frames are needed followed by well-supporting walkers. If there is mild-to-moderate flexion in hips and knees and correction of deformities of feet, this allows standing, transfers and, in individual cases, stepping in fully supported walkers, or with less support but in forearm-supporting walkers. The legs are sometimes more severe than the arms, so hands can be used with special controls for electronic communication equipment and electric wheelchairs. Children with tetraplegia may have good cognition, so focus on education and hand function warrants more time than the training of walking. However, there are adolescents who continue household walking with an appropriate walker for that environment. Surgery for knee flexion contractures is suggested by some surgeons for community walkers rather than for predominantly wheelchair users. Knee flexion surgery is discussed above.

Surgery for feet in all types of cerebral palsies depends on the other joint deformities. BTX A injection for plantar flexors with and without casting has been mentioned in this chapter, which delays surgery until children are over 6 years old. Surgeons may carry out lengthening of Achilles tendon (z-plasty) for gastrocnemius and soleus shortening or gastrocnemius slide. Surgery for varus or valgus may also involve tendon transfers. Surgery for equinus may be associated with surgery for other joint deformities. Post-operative physiotherapy may follow plasters, and strengthening is the main aim. Use of orthoses varies as how long a period they are worn in times of the day as there may be very weak muscles post-operatively, needing active strengthening. Several older children with more skeletal maturity may have various types of triple arthrodesis and some have peroneus brevis lengthening for valgus and transplants for equinovarus or varus. Various foot problems such as forefoot deformities are also treated by surgeons (Miller 2007). Post-operative physiotherapy for feet emphasises strengthening and training of standing and gait with correction of foot posture.

Therapy and daily care

(1) Positioning to stretch muscles in equipment and orthoses (braces) was used by Phelps (1952) and has become traditional with designs by many workers. However, the positioning equipment and orthoses have improved over the years. Today, a 24-hour postural management programme is planned which includes:

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