From an everyday clinical point of view, the management of cerebral palsy demands an understanding of the epilepsy which commonly co-occurs. A prelude to such management is ensuring the correctness of both the diagnosis of cerebral palsy and the diagnosis of epilepsy.
The definitions of epileptic seizures, symptomatic epileptic seizures, and epilepsy are as generally recognized (Stephenson, 1990; Engel & Pedley, 1997), as is the definition of anoxic seizures (Stephenson & McLeod, 2000). Movement disorders are paroxysmal disorders of movement which are the result neither of epileptic nor anoxic seizures.
Cerebral palsy is generally defined as ‘a persistent disorder of movement and posture caused by nonprogressive defects or lesions of the immature brain’ (Aicardi & Bax, 1998).
Clinical imitators of cerebral palsy
It is increasingly realized that what superficially appears to be cerebral palsy in an infant may be the result of a rare treatable biochemical error, such as glucose transporter (GLUT 1) deficiency, guanidinoacetate methyltransferase deficiency with creatine deficiency, argininemia, or one of the defects in serine biosynthesis. In all these conditions epileptic seizures may co-occur. Other rare biochemical mimics include disorders of purine and pyrimidine metabolism, and organic acid disorders such as 3-methylcrotonyl-CoA carboxylase deficiency.
Hyperekplexia is an example of an ion channelopathy in which the young infant is variably hypertonic, with non-epileptic convulsions giving profound syncopes.
The autosomal recessive Aicardi–Goutières syndrome may appear to be clinically static, but the cerebral lesions are slowly progressive.
We emphasize these points because the care of young patients with cerebral palsy is often undertaken by pediatricians with no special training in neurology.