Mathematics and reading disorders

Five to seven percent of children experience difficulties in learning mathematics and/or reading though they are not of low intelligence and do not suffer from educational deprivation (von Aster & Shalev Reference von Aster and Shalev2007; Wilson & Dehaene Reference Wilson, Dehaene, Coch, Dawson and Fischer2007). Current research suggests that these learning disabilities, known as developmental dyscalculia (DD) and dyslexia (for reading), are due to underlying brain dysfunctions (see, e.g., Cohen Kadosh et al. Reference Cohen Kadosh, Cohen Kadosh, Schuhmann, Kaas, Goebel, Henik and Sack2007; Kucian et al. Reference Kucian, Leoenneker, Dietrich, Dosch, Martin and von Aster2006; Shaywitz & Shaywitz Reference Shaywitz and Shaywitz2008). Similar to depression and generalized anxiety, DD and dyslexia, recognized psychiatric disorders (under different terms such as mathematics disorders or reading disorders; American Psychiatric Association 1994) are appropriate to test Cramer et al.'s main arguments.

It has been suggested that DD reflects deficiency mainly (but not only) in brain regions of the parietal cortex, along the intraparietal sulcus (IPS). IPS deficiencies can be found at the structural level (Isaacs et al. Reference Isaacs, Edmonds, Lucas and Gadian2001; Rotzer et al. Reference Rotzer, Kucian, Martin, von Aster, Klaver and Loenneker2008) and the functional level (e.g., DD in adults [Cohen Kadosh et al. Reference Cohen Kadosh, Cohen Kadosh, Schuhmann, Kaas, Goebel, Henik and Sack2007; Holloway & Ansari, in press]; DD in children [Kaufmann et al., in press; Kucian et al. Reference Kucian, Leoenneker, Dietrich, Dosch, Martin and von Aster2006; Mussolin et al., Reference Mussolin, De Volder, Grandin, Schlögel, Nassogne and Noël2010; Price et al. 2007]). The IPS is considered to be involved with an abstract, amodal representation of numbers (Cantlon et al. Reference Cantlon, Platt and Brannon2009; Dehaene Reference Dehaene2009). The IPS is also activated by numbers presented in symbolic notations such as Arabic numerals and spoken number words (Eger et al. Reference Eger, Sterzer, Russ, Giraud and Kleinschmidt2003). Despite indecisiveness in existent developmental imaging studies (e.g., Kucian et al. Reference Kucian, Leoenneker, Dietrich, Dosch, Martin and von Aster2006; Price et al. Reference Price, Holloway, Vesterinen, Rasanen and Ansari2007), deficiency in the IPS functioning is the best-validated core deficit or, in Cramer et al.'s terminology, the common cause of DD (Wilson & Dehaene Reference Wilson, Dehaene, Coch, Dawson and Fischer2007). This in itself does not fit the description of multiple behavioral symptoms organized in a connected network with no latent variable.

Importantly, the unique pathophysiology of DD is frequently accompanied by heterogeneous behavioral deficits. Moreover, this is the case in many other developmental disorders (Karmiloff-Smith Reference Karmiloff-Smith2006) – multiple problems are the rule, and pure disorders apply only to a minority of cases. Twenty to sixty percent of children with DD have associated learning problems such as dyslexia (von Aster & Shalev Reference von Aster and Shalev2007). What is the reason? We (Rubinsten & Henik Reference Rubinsten and Henik2009) have suggested two main alternative hypotheses for the origin of comorbidity of DD and dyslexia: (1) A single brain injury may cause DD and include a risk mechanism for dyslexia (see our Fig. 1, panel a). For example, a deficient ability to automatically associate written symbols with mental representations such as quantities or phonemes may lead to math and reading difficulties. In this case, a specific brain lesion produces a cognitive difficulty, and a network of symptoms may appear at the behavioral level but not necessarily at the cognitive or biological levels. (2) DD+dyslexia could be due to several brain dysfunctions – for example, one in the IPS (Price et al. Reference Price, Holloway, Vesterinen, Rasanen and Ansari2007) resulting in DD, and the second in the left peri-sylvian brain areas (McCandliss & Noble Reference McCandliss and Noble2003) resulting in dyslexia (see Fig. 1, panel b). Landerl et al. (Reference Landerl, Fussenegger, Moll and Willburger2009) have suggested that dyslexia and dyscalculia have separable cognitive profiles (i.e., a phonological deficit in dyslexia and a deficient number module in DD) that simply appear together. This does not support Cramer et al.'s network theory.

Figure 1.

Three alternative frameworks for the origins of comorbidities. IPS, intraparietal sulcus. (a) A unique pathophysiology resulting in a network of behavioral symptoms. (b) Multiple brain dysfunctions resulting in a network of behavioral symptoms and (c) A unique pathophysiology resulting in a behavioral disorder that is a risk mechanism for another disorder.

Attention-deficit hyperactivity disorder (ADHD)

One developmental disorder may be a risk mechanism for another; an example follows. ADHD is a neuropsychiatric disorder that is characterized by inattention, impulsivity, and motor restlessness (American Psychiatric Association 1994; Bush Reference Bush2010). Individuals with ADHD manifest unexpected problems in mathematics that cause impairments in academic achievement and daily functioning, with estimates ranging from 10% to 60% (Mayes et al. Reference Mayes, Calhoun and Crowell2000). Some attribute the significant mathematical delays in children with ADHD to attention-based impairments (Lindsay et al. Reference Lindsay, Tomazic, Levine and Accardo2001) or working memory (Rosselli et al. Reference Rosselli, Matute, Pinto and Ardila2006). These general cognitive impairments (i.e., not specific to mathematics) are considered to be integral features of the ADHD syndrome and, hence, may cause mathematical difficulties in some of these children (i.e., DD+ADHD) (Barkley Reference Barkley1997; Castellanos et al. Reference Castellanos, Sonuga-Barke, Milham and Tannock2006) (see Fig. 1, panel c).

To summarize, DD, dyslexia, and ADHD are specific neuro-developmental psychiatric disorders, but they are rooted at the biological and cognitive levels, and are only indicated by behavioral signs. Therefore, even if at present research regarding such biological and cognitive deficits is not always conclusive, it can better serve as a basis for testable predictions.