Why is it important to detect and define learning disability in a child, and how can one do so? The answers to the first question are, largely, not in dispute. Not only does the recognition and definition of learning disability contribute to our understanding of the basis of problems in a child's educational, developmental, and social progress, it also has significant long-term consequences, especially where the disability is more severe. The diagnosis or medical aetiology of the child's learning disability is a significant element of the story and carries major phenotypic implications, in terms of dysmorphology, organogenesis, development, and behaviour. It is one thing to diagnose, say, Down syndrome, and quite another to reach an accurate appraisal of the individual child's intellect, developmental attainments, and capacities. In turn, the definition of learning disability is not always straightforward and is sometimes quite controversial. This is partly because, traditionally, at least three different approaches are used to define learning disability in children, and each has its inherent attractions and pitfalls. These approaches are: definition by IQ alone; definition by IQ combined with social functioning and age at onset; and definition by service contact, the so-called ‘administrative definition’.

In 1937, Orton described children with motor coordination difficulties as ‘clumsy’, a term still used today. Other terms used to describe these difficulties include developmental dyspraxia, awkwardness, motor learning problems, and most recently, developmental coordination disorder (DCD). DCD is defined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) as a ‘marked impairment in the development of motor coordination [that]... interferes with academic achievement or activities of daily living’. The impaired coordination is present in the absence of a known medical condition such as cerebral palsy or muscular dystrophy. The heterogeneity of the motor and cognitive abilities of children included in this classification, and the numerous terms employed to describe them, have hindered systematic accumulation of knowledge about DCD.

Vitamin E (a-tocopherol) has antioxidant properties which prevent free radical damage to the nervous system, and there is a well-recognized association between vitamin-E deficiency and ataxia. This may result from such causes as malabsorption, the result of intestinal and liver disease, or severe malnutrition. There are also a number of hereditary conditions which can cause this deficiency. The classical abnormalities in fat-soluble vitamin-E deficiency progress from hyporeflexia, ataxia, limitation in upward gaze, and strabismus to long-tract defects, muscle weakness, visual field constriction, and centrocecal scotomata.