Hence, as no other MR-related measure discriminated between groups, counting-range slope findings seem to be related to inhibition ability and not to MR function. It is important to point out that there is substantial variation across studies in defining children with DD due to the fact that there is no agreed definition of DD. The range of cutoffs used to define DD in demographic studies ranges from performance

below the 3rd percentile to performance http://www.selleckchem.com/products/Perifosine.html below the 25th percentile (2SD–.68SD below the mean; for review see Devine et al., 2013). Here we used very stringent criteria to assure that children only had mathematical difficulties. We screened 1004 children and diagnosed DD if performance on two standardized mathematical measures was worse than 1SD while there was no ADHD and dyslexia, verbal IQ/reading was normal on four different tests and non-verbal IQ was normal on two tests. For example, Price et al. (2007) screened 55 children and WISC block-design performance differed by more than 1SD between DD and controls. In Piazza et al. (2010) about half the DD group was diagnosed with dyslexia. Mussolin et al. (2010a) screened 187 children and diagnosed DD if performance was worse than −1SD (15th percentile) on a multiplication test. However, multiplication relies heavily on verbal memory (Ashcraft, 1982). Mazzocco et al. (2011) screened

161 children and diagnosed 10 children below −1.3SD (10th percentile) with DD and children below −.65SD (25th percentile) as low maths achievers without MEK inhibitor using any other criteria. Various tests were used as covariates in analyses. However, the tests were recorded in various years during a 7-year long period and as noted above, ANCOVAs cannot ‘correct for’ major differences along independent variables (Miller and Chapman, 2001 and Porter and Raudenbush, 1987). Obviously, definition and measurement discrepancies can contribute to disagreeing findings across studies. In summary, there is evidence that IPS morphology and perhaps

function differ between DD and control participants Phosphoprotein phosphatase (Isaacs et al., 2001, Rotzer et al., 2008, Price et al., 2007 and Mussolin et al., 2010b). However, there is insufficient evidence for the argument that IPS dysfunction in DD can be linked to MR dysfunction: (1) Only one out of six fMRI studies found supporting behavioral data (Price et al., 2007). (2) The frequently used dot comparison task is seriously compromised by non-numerical confounds (Gebuis and Reynvoet, 2012 and Gebuis and Reynvoet, 2012; Szűcs et al., 2013). (3) Several behavioral and fMRI DD studies focusing on the MR theory of DD do not have non-numerical control conditions. (4) Adding to several negative findings (see above) our study used several measures of the MR but could not detect any clear MR impairment effects in DD.