Balance and reading are separate symptoms of dyslexia

Abstract

Research into dyslexia has been characterized by controversy, but the issue of balance and whether or not it should be seen as causal in dyslexia has been one of the most heatedly debated issues in recent years. The consensus of research into balance and dyslexia over a 20-year period has been that balance deficits may be identified in around 50% of a sample of children with dyslexia and around 20% of a sample of adults with dyslexia. It has also been argued that any evidence of balance deficits may be attributed to comorbid attention deficit in the participants with dyslexia studied. However, recent evidence from the Sheffield group has established that deficits may be found in adults if the level of difficulty is manipulated in dual task paradigms1 and has demonstrated that balance difficulties are found in children and adults with dyslexia with age-appropriate tests even when attention-deficit–hyperactivity disorder is controlled for.2 Balance deficits have been linked to the cerebellum in the cerebellar deficit hypothesis of dyslexia,3 which argues that both balance and reading deficits in dyslexia may be explained by differences in processing, based on cerebellar dysfunction. This is an explanatory theory which provides an independent explanation of the other major theories of dyslexia, in particular the phonological deficit and double-deficit theories of dyslexia. The cerebellar hypothesis itself has generated further controversy, in particular as to whether the cerebellum is a causal factor in dyslexia or whether it should be seen as simply an ‘innocent bystander’. The basis for these disputes rests on a simple misunderstanding and confusion between reading deficits and dyslexia. The cerebellar deficit claims only that the language-related regions of the cerebellum are affected in dyslexia. These are generally considered to be lobule VI and VIIB in the neocerebellum – well away from the motor and balance regions in the cerebellum. Other cerebellar regions may also be affected, but this is not necessary. The ontogenetic causal chain for dyslexia,3 which outlines development from birth to 8 years, makes it clear that balance deficits are not directly linked to reading deficits, because they involve a separate route in the causal chain. The cerebellar deficit hypothesis would therefore predict a higher incidence of balance difficulties in dyslexia, but that these would not necessarily be directly correlated with reading difficulties. The balance difficulties are best seen as symptoms of dyslexia which may be identified before children fail to learn to read, and which are therefore particularly useful in screening tests for dyslexia, such as the Dyslexia Early Screening Test.4 This is precisely the pattern which is identified in the family study by Viholainen et al.5 The incidence of balance deficits in children with family risk for dyslexia is significantly higher than controls, but reading deficits are more highly significant in this group. This study provides further confirmation of the importance of family studies in our understanding of dyslexia. More recent research has suggested that it may be fruitful to subsume the cerebellar deficit hypothesis within a ‘neural systems’ framework that attempts to capture disorders of learning at the level of the systems that work together, rather than the specific brain structures.6 This framework suggests that for dyslexia the neural system involved is the language-specific procedural learning system. The framework provides a natural explanation for the comorbidities found in dyslexia and it may have the potential to reunite the developmental disabilities.