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Cerebral palsy 

Cerebral palsy
Cerebral palsy

Ivan Donaldson

, C. David Marsden

, Susanne A. Schneider

, and Kailash P. Bhatia

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date: 03 July 2022

The term ‘cerebral palsy’ is loose and its boundaries are imprecise. It may be defined as a persisting, but not necessarily unchanging, acquired motor disturbance arising in the perinatal period or infancy, due to non-progressive brain damage. It embraces a wide variety of disorders with differing clinical features and aetiologies. A number of types of cerebral palsy can be distinguished, including 1) hemiplegic cerebral palsy, in which hemiparesis may be associated with other ipsilateral signs of corticospinal tract damage, 2) tetraplegic cerebral palsy, in which tetraparesis may be associated with signs of bilateral corticospinal tract damage, 3) diplegic cerebral palsy, in which weakness and other signs of corticospinal tract injury predominate in the lower limbs producing a picture resembling paraplegia, 4) ataxic cerebral palsy, in which cerebellar features predominate, and 5) dyskinetic cerebral palsy, in which involuntary movements are prominent. Individual patients often show a mixed picture. For example, cerebellar features, with ataxia may be associated with diplegia.

Dyskinetic cerebral palsy forms the basis of this chapter and other types of cerebral palsy are not discussed further, except to make occasional comparisons. Dyskinetic cerebral palsy can be caused by a number of acquired pathological processes, but the two main ones are perinatal hypoxia and jaundice. In addition, some cases that have been classifi ed under the rubric of cerebral palsy may actually have a genetic basis (Fletcher and Marsden 1996). The immediately following section on ‘Dyskinetic cerebral palsy’ deals with all causes of this disorder. Because kernicterus, resulting from neonatal jaundice, shows a number of additional features, these are elaborated separately in the next section entitled ‘Kernicterus’.

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