EDITORIAL

MOTOR D E W AND CEREBRAL PALSY 1 amused myself at a recent meeting by asking various colleagues what they thought was the most common motor disability in cerebral palsy. Pause while you think of your answer. Hemiplegia? Spastic diplegia? Oral problems, said one ingenious respondent, and maybe he was right. But the answer I was seeking was much more simple: it was ‘delay’.

The next question to ask, of course, is why is there delay? And again come the answers ‘because they have cerebral palsy’, ‘because they have spastic diplegia’. But is this right? I would submit that it is not. The child with spastic diplegia will walk abnormally, but the time at which he will walk, although associated with spastic diplegia, is due to the brain damage which causes motor delay. When they start to walk, children with spastic diplegia walk rather well in their own particular way.

Bleck’ reviewed the various studies of walking in cerebral palsy and showed that it is delayed in all forms, children with hemiplegia walking earliest, often between 18 and 24 months, and many of those with severe spastic quadriplegia not walking until later, or at all. His famous points system allows one to make a reasonable prediction for whether children with cerebral palsy will walk. It is worth noting that many of the movement patterns he looks at are not involved strictly with walking patterns e.g. the persistence of the asymmetric tonic neck reflex, or Moro response; so that delayed walking is associated with other abnormal signs within the central nervous system in relation to control of the motor system, but not to the actual abnormal neuromuscular activity in the legs themselves. With other subsystems, brain damage causes motor delay, but the association with age at walking is not a close one. Shapiro et al.’ conclude that motor development of profoundly mentally retarded children is variable. Cognition, they say, is less important than the basic neurological integrity in terms of the ability to walk: the more neurological signs they found the less likely was the child to walk. This suggests again that the degree of brain damage itself exercises some effect on the walking age.

Why should the extent of the brain damage have such effect? Although, as Thelen and Cooke’ have suggested, the new walk of the one-year-old is derived from a more simple patterning available from birth, the increase in complexity leads them to suggest further that the patterning of mature walking emerges from the ‘convergence of maturation and experience in all the contributing subsystems,

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including balance, posture control and strength, and the dynamic functional demands of upright locomotion. In short, we suggest that the details of the pattern generation are emergent with the task of walking and are not specified in detail beforehand’. If this account is correct, it is not surprising that the more neurological damage one can find clearly extending into more and more subsystems, the more difficult it is for the damaged brain to generate activity in the basic walking centre, hence delay and sometimes even failure to walk.

Clearly, we need the neurophysiologist to tell us much more about what is going on, but there are some implications, it seems to me, which are often neglected by clinicians. They tell parents that their child has cerebral palsy, and what they emphasise to them is the stiff-limbed (or dystonic) movements, the weakness, and the abnormal patterns of gait, but they do not emphasise the delay. Whereas parents of the mentally retarded child are told that the child is going to be slow-slow at everything-and the family accepts, albeit with difficulty, that nothing can hasten the onset of waIking and other skiIls. I beIieve this is a message that few families of children with cerebral palsy receive from their clinicians and in consequence the parents are desperately looking for a form of therapy which will get the child walking.

What we should be aiming to achieve is the removal of emphasis from the time of walking and instead greater effort in ensuring that when walking does occur it is as normal as possible. This is why the early management of the child is important. We can prevent those tight hamstrings and achilles tendons, so that the child may begin to walk as normally as possible. By strenuously exercising normal babies one can, it is said, get walking to occur a little earlier. No doubt the same is true for a cerebral palsied child, but that should not be the principal aim of therapy.

MARTIN BAX

References 1. Bleck, E. E. (1987) Orthopaedic Management in Cerebral Palsy. Clinics in Developmental Medicine, Nos.

2 . Shapiro, B. K . , Accardo, P. J . , Capute, A. J . (1979) ‘Factors affecting walking in a profoundly retarded

3. Thelen, E. , Cooke, D. W . (1987) ‘Relationship between newborn stepping and later walking: a new

991100. London: Mac Keith Press with Blackwell Scientific; Philadelphia: Lippincott. p. 122.

population.’ Developmental Medicine and Child Neurology, 21, 369-373.

interpretation.’ Developmental Medicine and Child Neurology, 29, 380-393.

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