Brain damage in cerebral palsy may also be responsible for special sense defects of vision and hearing, abnormalities of speech and language, and aberrations of perception (Hall 1984; Neville 2000). Included in the perceptual defects are the agnosias. The agnosias are difficulties in recognising objects or symbols, even though sensation as such is not impaired, and the patient can prove by other means to know or have known what the object or symbol is. There may also be dyspraxias, some of which are also called visuomotor defects. This means that the child is unable to perform certain movements even though there is no paralysis, because the patterns or engrams have been lost or have not developed. Dyspraxia can involve movements of the limbs, face, eyes, tongue or be specifically restricted to such acts as writing, drawing and construction or even dressing. In other words, there seems to be a problem in ‘motor planning’ in those children who are dyspraxic. Some children may also have various behavioural problems such as distractibility and hy-perkinesis, which are based on the brain damage. All these defects result in various learning problems and difficulties in communication. In addition, there may be intellectual impairment and various epilepsies (Himmelmann et al. 2006).

Not every child has some or all of these associated impairments. Even if the impairment were only motor, the resulting paucity of movement would prevent the child from fully exploring the environment. He is therefore limited in the acquisition of sensations and perceptions of everyday things. A child may then appear to have defects of perception, but these may not be due to the brain damage but caused by lack of experience. The same lack of everyday experiences retards the development of language and affects the child’s speech. His general understanding may suffer, so he appears to be intellectually retarded. This can go so far that normal intelligence has been camouflaged by severe physical disability. Furthermore, the lack of movement can affect the general behaviour of the child. Thus, some abnormal behaviour may be due to the lack of satisfying emotional and social experiences for which movement is necessary. Motor dysfunction may therefore interact with emotional and social development of a child. However, positive attitudes in a family and child can encourage optimum development.

Teamwork. It is therefore important for any therapist to recognise that motor function cannot be isolated from other functions and that she is treating a child who is not solely physically but multiply disabled. Therapists will also need to consider when the associated physical and behavioural problems constrain motor function (Thylefors et al. 2000).

In order to manage the multiple disabilities and lack of related learning experiences which interfere with a child’s development, a physiotherapist or occupational therapist needs to be part of a team. The teamwork varies in different places such as community centres, child development centres, units in hospitals or within educational settings. Teamwork is discussed in Chapters 2, 8, 10 and 12.

Premature infants are at greater risk of brain dysfunction. There are many causes of the brain damage, including abnormal development of the brain, anoxia, intracranial bleeding, excessive neonatal asphyxia (hypoxic ischaemic neonatal encephalopa-thy), trauma, hypoglycaemia, anoxia as in near-drowning, choking, neurotrophic virus and from various infections. These have been extensively discussed in the medical literature (Rosenbloom 1995; Hagberg et al. 1996; Stanley et al. 2000; Himmel-mann et al. 2005). The therapist is, however, rarely guided by the aetiology in her treatment planning. In some cases the cause is not certain, and in many cases knowing the cause does not necessarily indicate a specific diagnosis or specific treatment. Nevertheless, the therapist should acquaint herself with the history of the case. Many of these children have been affected from infancy and have been difficult to feed and handle. Many hospitalisations and separations of babies from parents may happen in the early period. This may easily have influenced the parent–child relationships so essential for child development. Furthermore, the history may sometimes give an indication of the prognosis; for example, with marked microcephaly with severe multiple impairments the prognosis would be poor.

It is important to recognise that the causes of cerebral palsy take place in the prenatal, perinatal and postnatal periods. In all cases, it is an immature nervous system which suffers the insult and the nervous system afterwards continues to develop in the presence of the damage. The therapist must therefore not think of herself as treating an upper motor neurone lesion in a ‘little adult’ nor can she regard the problem solely as one of retardation in development. What the therapist faces is a complex situation of pathological symptoms within the context of a developing child (Sheridan 1975, 1977; Drillien & Drummond 1977, 1983; Illingworth 1983; McGraw 1989; Sheridan et al. 2008). There are six main aspects to the clinical picture:

In order to recognise abnormal motor and general behaviour, the therapist should know what a normal child does and how he does it at the various stages of his development. Information on each individual child’s developmental levels should be sought from the consultants and other members of the cerebral palsy team. Reference will have to be made to the extensive literature on the field of child development.

Although normal child development is the basis on which the abnormal development is appreciated, it does not follow that assessment and treatment should rely upon a strict adherence to normal developmental schedules. Even ‘normal’ children show many variations from the ‘normal’ developmental sequences and patterns of development which have been derived from the average child. Cultural differences exist for normal motor development (Solomons & Solomons 1975; Hopkins & Westra 1989). However, in any culture, the child with cerebral palsy will show additional variations due to neurological and mechanical difficulties. If one considers, say, the normal developmental scales of gross motor development, in cerebral palsy a child has frequently achieved abilities (components) and motor functions at one level of development, omitted abilities at another level and only partially achieved motor abilities and functions at still other levels. There is thus more of a scatter of abilities and whole motor functions than in able-bodied children. The analysis of motor function into components is discussed in Chapters 5, 6, 8 and 9.

If the gross motor development is generally considered to be around a given age, the development of hand function, speech and language, social and emotional and intellectual levels may all be at different ages. None of these ages may necessarily coincide with the child’s chronological age.

Therefore, the developmental schedules in normal child development should only be used as guidelines in treatment, and adaptation should be made for each child’s disabilities and individuality (see Chapter 9).

More attention is usually given to motor development rather than other avenues of development, as it is the motor dysfunction which characterises cerebral palsy. Here again, the therapist should remember that abnormal motor behaviour interacts with other functions. Each area of development – such as gross motor, manipulation, speech and language, perception, social and emotional adjustments, and cognition – interacts as well as has its own pattern or avenue of development. Furthermore, the potential for function is dependent not only on the disabilities present but also on a child, his personality and ‘drive’ as well as his capacity to learn. Therefore, a total habilitation programme is necessary and should be planned to deal with the whole development of each child.

Whilst aiming at the maximum function possible, the therapists concerned must take account of the damaged nervous system and adjust their expectations of achievements by the child. This depends on a therapist’s clinical experience as prognosis is difficult in view of the multiple factors involved. There are measures of the severity of a child’s disability in Chapter 8, which guide the expectations of a therapist, but overdependence on levels of severity may not always be reliable in individual children.

Change in clinical picture

As the lesion is in a developing nervous system, the clinical picture is clearly not a static set of signs and symptoms for treatment. But whilst the lesion itself is non-progressive, its manifestations change as the nervous and musculoskeletal systems mature. As more is demanded of the child, the degree of the motor disability appears to be greater. For example, a 3-year-old is expected to do more than a baby, and therefore his difficulties are greater for the same pathology.

In addition, the pathological symptoms may develop with the years. Spasticity may increase, involuntary movements may only appear at the age of 2 or 3 years and ataxia may only be diagnosed when the child walks or when grasp is expected to become more accurate. Diagnoses may change as the baby develops to childhood, and especially as the child becomes more active. For example, a mono-plegia reveals itself as a hemiplegia. Later a triplegia reveals itself as a tetraplegia. Cerebral palsies have an emerging diagnosis. Later, especially in adolescence, growth and increase in weight contribute to apparent deterioration. Recent research identifies that deterioration is not inevitable in all cases (see Chapter 7).

Treatment and management in infancy. The earlier the treatment is started, the more opportunity is given for whatever potential there may be for developing any normal abilities and for decreasing the abnormal movement patterns and postural difficulties (Kong 1987; de Groot 1993). However, abnormalities detected in infants may be transient as some infants overcome them without intervention. Therapists offer pleasurable and a variety of developmentally appropriate and active motor activities enjoyed by both parent and baby. During intervention, therapists observe if a baby or young child makes his own efforts to move using compensatory or adaptive patterns which can be ‘good enough’ but block the development of more efficient patterns or result in ‘learned disuse’ of a body part. Any immobility threatens musculoskeletal growth and development which can lead to deformities. Early physiotherapy minimises such problems.

The value of early developmental intervention is to provide an increase in a baby’s sensory-motor and everyday experiences and interaction with his mother and father. The sooner a baby can be helped to move, the sooner he can explore and the sooner he can communicate the information he gains through such exploration. The therapist is in fact contributing to his learning and understanding as well as enabling him to bond with his mother and father.

Although the clinical picture is known to change with the years, it is not yet possible to predict the natural history of the condition in each particular child. Infants and babies with marked early neurological signs may later prove to be only mildly affected, or even normal (Ellenberg & Nelson 1981; Nelson & Ellenberg 1982). On the other hand, apparently mildly affected ones may become progressively worse with the years. It is therefore difficult to prove the value of a number of different early treatment approaches (Vojta 1984; Kong 1987; Katona 1989; Morris 1996). However, research in neonatal physiotherapy continues. Blauw-Hospers and Hadders-Algra (2005) have found positive effects on babies at term, rather than preterm, with specific and general developmental early treatments in their systematic review of 12 studies. The review by Spittle et al. (2007) found little evidence of early intervention on motor development. Reviews point out that the studies involve heterogeneous samples.

Nevertheless, until we know more definitely which babies are going to ‘come right’ on their own, it is better to let them have the benefit of treatment so that any potentials for improvement are not lost. Despite the controversy as to the value of early treatment, there is clearly no doubt about its importance to the parents, who receive a great deal of practical advice and support from the therapists. Among others, Goodman et al. (1991) found that if their research could not firmly state that neonatal physiotherapy was responsible for babies’ motor developmental progress, all mothers confirmed their great appreciation for the support and practical ideas from their physiotherapists. Olow (1986) emphasises that early intervention reduces the frustration of early rearing of children with disabilities. Whilst medical practitioners are watching the development of the child in order to make a reliable diagnosis, the parents have to live with that child throughout each day of those months and years. Parents need support and practical ideas for feeding, child-care and motor activities for their child throughout the emerging diagnoses. This is an essential part of the therapist’s management programme with them. Well-supported parents are most likely to benefit their young children’s development (see Chapter 2).

Treatment and management in childhood, adolescence and adulthood. During these changes in the clinical picture, treatment and management programmes need to relate to an individual’s wider environments of the playgroup, nursery, preschool, schools, adult day care centres and work places. The persons with cerebral palsy at different ages also change through interaction with the variety of personnel in environments in which they find themselves. Physiotherapy and occupational therapy as well as other therapies are therefore being planned across a lifespan of each person with cerebral palsy. Management will include working with orthotists, orthopaedic surgeons and other consultants. The therapist will share selected skills and advice on equipment with anybody closely involved with each person having a disability.

Numerous classifications and subclassifications have been proposed by different authorities, and though clinically helpful, none of these diagnostic labels suffice to formulate adequate treatment plans. The therapist must also have a detailed assessment based primarily on motor functions in order to work out a treatment programme.

Classifications of topography of cerebral palsy

The topographical classifications frequently used are as follows:

Tetraplegia (quadriplegia). Involvement of all limbs and body. Arms are equally or more affected than the legs. Many are asymmetrical (one side more affected).

Diplegia. Involvement of limbs, with arms much less affected than legs. Asymmetry may be present.

Hemiplegia. Limbs and body on one side are affected.

Neville and Goodman (2001) present different authors in a book on congenital hemiplegia. These topographical classifications can be imprecise, as they may change with a child’s development. One useful upper limb may convey a triplegia which could become a tetraplegia. Upper limbs may appear unaffected, suggesting a paraplegia but being really a diplegia with only fine-hand use being affected when this is later expected. Hemiplegia may have minor involvement on the unaffected side. A monoplegia is rare, usually becoming a hemiplegia with increased activity.

Classification of types of cerebral palsies

There are spastic types, athetoid (dyskinetic) types and a rare ataxic type. There is a hypotonic type which either becomes a spastic, athetoid or ataxic type. There is a transient dystonic stage in babies before they are diagnosed as a spastic or dyskinetic type of cerebral palsy (Bax & Brown 2004). Tetraplegias usually have either spasticity, dystonia, dyskinesia (athetosis), hypotonia or ataxia. Hemiplegia is usually a spastic type often starting out hypotonic. Hemi-athetoids with or without dysto-nia are occasionally seen. Once again, classifications are not always clear-cut and the therapist may have to treat impairments of one type in another type. The predominant impairments will contribute to the diagnostic type referred for therapy. Developmental functional training is nevertheless indicated for all types of cerebral palsies.

Main motor characteristics are as follows:

Hypertonus. If spastic muscles are stretched at a particular speed, they respond in an exaggerated fashion. They contract, blocking the movement. If this sudden passive stretch is continued, the spas-ticity may melt away in some cases. The movement block is the ‘catch’ and with the subsequent movement this is called a ‘clasp-knife’ variety of spastic hypertonus. This hyperactive stretch reflex may occur at the beginning, middle or near the end of the range of movement. There are increased tendon jerks, occasional clonus and other signs of upper motor neurone lesion. The velocity-dependent hyperactive stretch reflex is the physiological definition of spasticity. Stiffness is not true spasticity and may or may not accompany the reflex reaction to brisk passive stretch. Viscoelastic muscle and soft tissue changes are also causes of stiffness (Katz & Rymer 1989; Dietz & Berger 1995). However, clinicians usually use ‘spasticity’ and ‘spastic muscles’ as an umbrella term for stiffness of limbs and recognise that other motor symptoms are also included under this umbrella. These are discussed below. Current views are that the hyperactive stretch reflex is not as much the cause of abnormal function as weakness (Lin 2004; Ross & Engsberg 2007). Movements are usually slower than the velocity needed to obtain the hyperactive stretch reflex.

Hypertonus may be either spasticity or rigidity (dystonia). The overlap between the two is almost impossible to differentiate when severe. A mixture of spasticity and rigidity may be diagnosed (Lin 2004). Rigidity is recognised by a plastic or continuous resistance to passive stretch throughout the full range of motion. This lead-pipe rigidity differs from spasticity as spasticity offers resistance at a point or small part of the passive range of motion. Spasticity is selective affecting specific muscles, for example giving a predominantly flexor pattern in the arm and extensor pattern in the leg. Rigidity (dystonia) affects all muscle groups equally. Drugs such as bo-tulinum toxin A, oral and intrathecal baclofen are used to control spasticity and dystonia (Lin 2004), together with a physiotherapy programme.