Abstract:

Developmental dyslexia (hereafter referred as "dyslexia") will not only affect the lifelong development of individuals but also impose an additional financial burden on society. Digging into the relevant neural mechanisms contributes to the early prediction and intervention of dyslexia. Established models of the neural bases of dyslexia primarily focused on the cerebrum. In recent years, extensive studies have shown that dyslexia is also associated with cerebellar abnormalities. However, it remains unclear about the relationships between the two.

By summarizing recent findings, we found that the cerebellum could play multiple roles in reading. First, it could influence reading in different ways. Cerebellar dysfunctions could impair reading by affecting motor or motor-related skills (such as oculomotor control, automatization, or articulation), or by disturbing linguistic-related processes (such as phonological or semantic processing). Second, different subtypes of dyslexia are associated with abnormalities in distinct cerebellar regions. For example, dyslexic readers with automatization deficits showed abnormal neural activities in the anterior parts of the cerebellum, which were responsible for motor processing, whereas dyslexic readers suffering from visual and phonological deficits were associated with the abnormalities in the gray matter volume of the posterolateral areas of the cerebellum, which were mainly responsible for high-level cognitive processing. These results indicate that the relationship between dyslexia and the cerebellum is not unitary. There may exist multiple cerebellar areas being targeted by dyslexia, which also contribute differently to reading.

The causal relationships between cerebellar abnormalities and dyslexia might be bi-directional. Previous literature found that structural deficits in the posterolateral parts of the cerebellum were only associated with dyslexia compared to other development disorders (i.e., ADHD, autism) that may coexist with dyslexia. This result suggests that neural abnormalities in these areas were due to deficits in reading abilities rather than other comorbidities. Additionally, these regions vary in their causal relationships with dyslexia. For example, activation in the anterior parts of the right lobule VI, responsible for motor processing, showed greater activation or functional connectivity with the cerebrum in dyslexic readers compared to normal readers. These increased neural activities may be the compensatory mechanisms of dyslexia and a by-product of reading difficulties. In contrast, neural activities of the cerebellar areas responsible for linguistic processing (i.e., the right lobule VII) could predict future reading abilities, indicating that the functional state of the cerebellum in early developmental stages may influence reading development. Moreover, functional deactivations in the cerebellar linguistic areas have been observed in preschool readers with a high risk of dyslexia, suggesting that cerebellar abnormalities have occurred before formal reading instruction. These results jointly support that cerebellar abnormalities may be the cause of dyslexia.

The results mentioned above illustrate that the cerebellum is more than a reading-related hub. There could be multiple cerebellar regions that are engaged in reading, with different regions supporting different cognitive processes and having distinct causal relationships with dyslexia. Accordingly, we introduced the "cerebro-cerebellar mapping hypothesis of word reading", which proposed that reading-related regions in the cerebellum map to their functional correspondence areas in the cerebrum. Regions with the same functions across the cerebrum and cerebellum synchronized in neural activities and collaborated during reading. Dysfunctions of this collaboration may lead to dyslexia. This new framework aims to reveal the relationship between reading, the cerebellum, and the cerebrum from a new perspective, and offers important insights into the neural mechanism of dyslexia and the role of the cerebellum in high-level cognitive processing.

Key words: developmental dyslexia, cerebellar abnormalities, the neural mechanisms of reading, mapping hypothesis, causal relationship