Dyslexia is a reading disorder wherein an individual experiences trouble with reading. Individuals with dyslexia have normal levels of intelligence but can exhibit difficulties with spelling, reading fluency, pronunciation, "sounding out" words, writing out words, and reading comprehension. The neurological nature and underlying causes of dyslexia are an active area of research. However, some experts believe that the distinction of dyslexia as a separate reading disorder and therefore recognized disability is a topic of some controversy.
History
Dyslexia was first identified by Oswald Berkhan in 1881, and the term 'dyslexia' later coined in 1887 by Rudolf Berlin, an ophthalmologist practicing in Stuttgart, Germany.
During the twentieth century, dyslexia was primarily seen as a phonological deficit (specifically phonological awareness) that resulted in a reading deficit. Dyslexia was seen as an issue with reading achievement specifically, caused by deficits in discrimination of written word sounds as opposed to a broader disorder of brain function. However, much research from the 1990s onward has focused on the potential biological bases of dyslexia and understanding dyslexia as a disorder of brain function. One of the first weaknesses of the strictly phonological deficit hypothesis for dyslexia was its inability to account for the genetic link of dyslexia. Specifically, it's been shown that "Relatively high heritabilities were observed for both reading ability and dyslexia indicating substantial genetic influences." In a large twin study (sample 1031 twins), Gayan and Olson established that dyslexia was highly heritable, while a family study by Pennington (sample 1698 individuals) showed familial risk rates of 35-45%.
Without a biological explanation for dyslexia, this heritability went unexplained. Not only must the heritability be explained, but also the environmental factors that protected at-risk children from developing dyslexia. Research began to focus on potential biological causes and to center the study of dyslexia in a developmental framework. A second major weakness of the strictly phonological deficit hypothesis was its strict definition of dyslexia as a reading disorder. Consequently, the various secondary symptoms were unable to be explained, including automatization deficits of both skill and knowledge acquisition, balance impairments, motor skill/writing deficits, and muscle tone underdevelopment. New theories of dyslexia began to be a focus of research, with the most well established being the magnocellular deficit theory the automatization deficit theory, and the double-deficit hypothesis.
Theories
Theories of the etiology of dyslexia have and are evolving with each new generation of dyslexia researchers, and the more recent theories of dyslexia tend to enhance one or more of the older theories as understanding of the nature of dyslexia evolves.
Theories should not be viewed as competing, but as attempting to explain the underlying causes of a similar set of symptoms from a variety of research perspectives and background.
Cerebellar theory
The cerebellar theory of dyslexia asserts that the cause of dyslexia is an abnormality in the cerebellum (a region in the back of the brain), which in turn cause disruption in normal development, which causes issues with motor control, balance, working memory, attention, automatization, and ultimately, reading. This theory was initially proposed by Harold Levinson and Jan Frank in 1973 and further developed by Levinson and other researchers. Angela Fawcett and Rod Nicolson later proposed that the cerebellum contributes to motor control during the articulation of speech, and that articulation problems can contribute to the phonological processing deficits that can cause dyslexia. They also reasoned that the cerebellum contributes to the automatisation of learned behaviors, which may include learning the grapheme-phoneme relationships when reading text.