Abstract
Botulinum toxin is now routinely used in adult focal dystonias,1 including blepharospasm,2 spasmodic torticollis,3 and hemifacial spasm, and also in squint and some types of tremor.4 When injected close to the main area of nerve arborisation within a muscle, the toxin is selectively taken up by cholinergic nerve terminals and blocks neuromuscular transmission for between two and four months until new terminals grow. Recent reports of its use in the cerebral palsies are encouraging but need to be placed in context. The cerebral palsies are motor disorders arising from static brain abnormalities that may result from early embryological defects or damage in utero or early extrauterine life. Cerebral palsy phenotypes often include primary cognitive, psychiatric, sensory, and seizure disorders and a wide range of secondary skeletal and general medical illnesses. The motor disorders vary greatly in severity and neurological signs. Each pathology may therefore cause a range of types of cerebral palsy without any necessary concordance between pathological and clinical categories.5 The process of progressive developmental revelation with age, the cascade of disabilities in the first two to three decades, and the propensity of the developing nervous system to compensate for early damage (albeit by its …
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