By Alon Seifan, MD, MS
Assistant Professor of Neurology, Weill Cornell Medical College, Memory Disorders Program

Dr. Seifan reports no financial relationships relevant to this field of study.

Synopsis: Neuroanatomical differences in primary sensory cortices may distinguish dyslexic individuals from non-dyslexic individuals, providing a potential biomarker for identifying adults who may be predisposed to developing atypical neurodegenerative disease.

Source: Clark KA, et al. Neuroanatomical precursors of dyslexia identified from pre-reading through to age 11. Brain 2014;137:

Developmental dyslexia is a reading disorder characterized by difficulty in learning to decode print. According to the revised Diagnostics and Statistics Manual – V criteria for specific learning disabilities (SLD), dyslexia is one of three specific learning disabilities. SLDs can manifest as impairment of reading, writing, or math. Individuals with dyslexia, now called “SLD with impairment in reading,” have reading difficulties that persist despite targeted instruction, with skills substantially below those expected for age, causing functional disability. Onset is almost always during the school-age years. For a diagnosis of SLD, concomitant intellectual disabilities and attention deficit hyperactivity disorder (ADHD) should not be present.

The prevalence of dyslexia is estimated at 7%. Dyslexia is a constitutional condition, implying a predisposition beginning at birth. Reading requires higher-level cognitive processes such as integration of basic sensory information, as well as lower-level processes such as those related to basic sensory input. Most individuals with dyslexia display difficulty with phonological awareness, rapid naming, and verbal working memory, all of which are necessary for reading ability. Structural and functional imaging studies across alphabetic languages consistently reveal alterations in gray matter and white matter in affected individuals, specifically within the left posterior language system. However, despite decades of research, it remains unclear which brain differences represent the cause of behavioral difficulties in dyslexia and which result from reduced reading experience. To answer these types of questions, longitudinal studies of preliterate children are required.

The recent study by Clark et al specifically uses a longitudinal approach to identify brain differences that could predate literacy acquisition. The goal was to quantify how cortical thickness evolved over time, with the first magnetic resonance imaging (MRI) measurement taken at age 6, which is 1 year prior to the age that children learn to read. The study initially recruited 52 children to be followed longitudinally with neurocognitive and structural MRI measurements taken from preschool to age 11 years; 39 of these children participated in the study. Subjects with high and low risk for dyslexia were chosen from a cohort of Norwegian children who were part of the Bergen Longitudinal Dyslexia Study. Individuals with mental retardation, ADHD, or other neurological impairment (including vision or hearing impairment) were excluded. Dyslexia was defined as scoring below the 25th percentile in two or more literacy tests. Using this definition, 11 subjects were ultimately diagnosed with dyslexia.

At the first MRI at age 6 years, children who were later diagnosed with dyslexia, as compared to those who were not, showed significantly thinner cortex in five regions of interest, some of which subserve primary sensory processes and others higher-level associative processes. Specifically, thinner cortex was observed in primary auditory and visual cortex (Heschl’s and lingual gyri, respectively), and in heteromodal cortex (middle cingulate, medial frontal, and orbitofrontal gyri). By the time the children had learned to read, cortical thickness differences were no longer apparent in any of the regions except Heschl’s gyrus, which remained significantly thinner in dyslexics vs controls. This implies the presence of reduced neuroanatomical capacity to process auditory information in children destined for dyslexia and does not fully normalize with reading acquisition. The study suggests that atypical development of primary sensory cortex, particularly within Heschl’s gyrus, is fundamental to the reading deficits and related cortical differences observed in some dyslexics.


Despite almost 100 years of research into dyslexia, consensus regarding the underlying pathology has been difficult to achieve. Studies have often conflicted regarding specific location of abnormality, probably because the dyslexia reality represents a heterogeneous group of related disorders. For example, there appear to be at least two subgroups, one with primarily sublexical impairment (poor non-word reading) and another subgroup with primarily lexical impairment (poor irregular word reading); mixed lexical and sublexical subtypes also exist. Complicating matters further, reading disabilities are often comorbid with math disabilities, ADHD, and other language disorders. The study by Clark et al did well to exclude individuals with ADHD and intellectual disabilities, but did not take into account comorbidity with other SLDs such as dyscalculia. Thus, the extent to which the findings are specific to SLD with reading impairment remains unknown.

Another common challenge regarding neuroimaging studies of dyslexia, and particularly with meta-analyses, is the fact that individuals with similar ages can often be at quite different developmental stages. Major developmental changes are occurring even on a year-to-year basis in children, so studies (in particular, meta-analyses) that combine children into age groups may miss important developmental changes. The study by Clark et al avoids this problem by imaging the children at specific ages, but the presence of individual-level variation in developmental trajectories could still confound the findings. Another important thing to note is the fact that although children had not learned to read independently until age 7 years, the initial MRI measurements at age 6 may reflect neuroanatomical changes from pre-literacy training, including years of exposure to print and reading. Longitudinal imaging studies of dyslexia can help us to understand which brain differences cause dyslexia and which result from impaired reading experience.