Increased structural covariance in brain regions for number processing and memory in children with developmental dyscalculia.

Developmental dyscalculia (DD) is a developmental learning disability associated with deficits in processing numerical and mathematical information. Several studies demonstrated functional network alterations in DD. Yet, there are no studies, which examined the structural network integrity in DD. We compared whole-brain maps of volume based structural covariance between 19 (4 males) children with DD and 18 (4 males) typically developing children. We found elevated structural covariance in the DD group between the anterior intraparietal sulcus to the middle temporal and frontal gyrus (p < 0.05, corrected). A hippocampus subfield analysis showed higher structural covariance in the DD group for area CA3 to the parahippocampal and calcarine sulcus, angular gyrus and anterior part of the intraparietal sulcus as well as to the lingual gyrus. Lower structural covariance in this group was seen for the subiculum to orbitofrontal gyrus, anterior insula and middle frontal gyrus. In contrast, the primary motor cortex (control region) revealed no difference in structural covariance between groups. Our results extend functional magnetic resonance studies by revealing abnormal gray matter integrity in children with DD. These findings thus indicate that the pathophysiology of DD is mediated by both structural and functional abnormalities in a network involved in number processing and memory function.

Neurostructural correlate of math anxiety in the brain of children.

Adequate mathematical competencies are currently indispensable in professional and social life. However, mathematics is often associated with stress and frustration and the confrontation with tasks that require mathematical knowledge triggers anxiety in many children. We examined if there is a relationship between math anxiety and changes in brain structure in children with and without developmental dyscalculia. Our findings showed that math anxiety is related to altered brain structure. In particular, the right amygdala volume was reduced in individuals with higher math anxiety. In conclusion, math anxiety not only hinders children in arithmetic development, but it is associated with altered brain structure in areas related to fear processing. This emphasizes the far-reaching outcome emotional factors in mathematical cognition can have and encourages educators and researchers alike to consider math anxiety to prevent detrimental long-term consequences on school achievement and quality of life, especially in children with developmental dyscalculia.

Probing the nature of deficits in the 'Approximate Number System' in children with persistent Developmental Dyscalculia.

In the present study we examined whether children with Developmental Dyscalculia (DD) exhibit a deficit in the so-called 'Approximate Number System' (ANS). To do so, we examined a group of elementary school children who demonstrated persistent low math achievement over 4 years and compared them to typically developing (TD), aged-matched controls. The integrity of the ANS was measured using the Panamath (www.panamath.org) non-symbolic numerical discrimination test. Children with DD demonstrated imprecise ANS acuity indexed by larger Weber fraction (w) compared to TD controls. Given recent findings showing that non-symbolic numerical discrimination is affected by visual parameters, we went further and investigated whether children performed differently on trials on which number of dots and their overall area were either congruent or incongruent with each other. This analysis revealed that differences in w were only found between DD and TD children on the incongruent trials. In addition, visuo-spatial working memory strongly predicts individual differences in ANS acuity (w) during the incongruent trials. Thus the purported ANS deficit in DD can be explained by a difficulty in extracting number from an array of dots when area is anti-correlated with number. These data highlight the role of visuo-spatial working memory during the extraction process, and demonstrate that close attention needs to be paid to perceptual processes invoked by tasks thought to represent measures of the ANS.

Brain hyper-connectivity and operation-specific deficits during arithmetic problem solving in children with developmental dyscalculia.

Developmental dyscalculia (DD) is marked by specific deficits in processing numerical and mathematical information despite normal intelligence (IQ) and reading ability. We examined how brain circuits used by young children with DD to solve simple addition and subtraction problems differ from those used by typically developing (TD) children who were matched on age, IQ, reading ability, and working memory. Children with DD were slower and less accurate during problem solving than TD children, and were especially impaired on their ability to solve subtraction problems. Children with DD showed significantly greater activity in multiple parietal, occipito-temporal and prefrontal cortex regions while solving addition and subtraction problems. Despite poorer performance during subtraction, children with DD showed greater activity in multiple intra-parietal sulcus (IPS) and superior parietal lobule subdivisions in the dorsal posterior parietal cortex as well as fusiform gyrus in the ventral occipito-temporal cortex. Critically, effective connectivity analyses revealed hyper-connectivity, rather than reduced connectivity, between the IPS and multiple brain systems including the lateral fronto-parietal and default mode networks in children with DD during both addition and subtraction. These findings suggest the IPS and its functional circuits are a major locus of dysfunction during both addition and subtraction problem solving in DD, and that inappropriate task modulation and hyper-connectivity, rather than under-engagement and under-connectivity, are the neural mechanisms underlying problem solving difficulties in children with DD. We discuss our findings in the broader context of multiple levels of analysis and performance issues inherent in neuroimaging studies of typical and atypical development.

Dyscalculia, dysgraphia, and left-right confusion from a left posterior peri-insular infarct.

The Gerstmann syndrome of dyscalculia, dysgraphia, left-right confusion, and finger agnosia is generally attributed to lesions near the angular gyrus of the dominant hemisphere. A 68-year-old right-handed woman presented with sudden difficulty completing a Sudoku grid and was found to have dyscalculia, dysgraphia, and left-right confusion. Magnetic resonance imaging (MRI) showed a focus of abnormal reduced diffusivity in the left posterior insula and temporoparietal operculum consistent with acute infarct. Gerstmann syndrome from an insular or peri-insular lesion has not been described in the literature previously. Pathological and functional imaging studies show connections between left posterior insular region and inferior parietal lobe. We postulate that the insula and operculum lesion disrupted key functional networks resulting in a pseudoparietal presentation.

Residual number processing in dyscalculia.

Developmental dyscalculia - a congenital learning disability in understanding numerical concepts - is typically associated with parietal lobe abnormality. However, people with dyscalculia often retain some residual numerical abilities, reported in studies that otherwise focused on abnormalities in the dyscalculic brain. Here we took a different perspective by focusing on brain regions that support residual number processing in dyscalculia. All participants accurately performed semantic and categorical colour-decision tasks with numerical and non-numerical stimuli, with adults with dyscalculia performing slower than controls in the number semantic tasks only. Structural imaging showed less grey-matter volume in the right parietal cortex in people with dyscalculia relative to controls. Functional MRI showed that accurate number semantic judgements were maintained by parietal and inferior frontal activations that were common to adults with dyscalculia and controls, with higher activation for participants with dyscalculia than controls in the right superior frontal cortex and the left inferior frontal sulcus. Enhanced activation in these frontal areas was driven by people with dyscalculia who made faster rather than slower numerical decisions; however, activation could not be accounted for by response times per se, because it was greater for fast relative to slow dyscalculics but not greater for fast controls relative to slow dyscalculics. In conclusion, our results reveal two frontal brain regions that support efficient number processing in dyscalculia.

Developmental dyscalculia: a dysconnection syndrome?

Numerical understanding is important for everyday life. For children with developmental dyscalculia (DD), numbers and magnitudes present profound problems which are thought to be based upon neuronal impairments of key regions for numerical understanding. The aim of the present study was to investigate possible differences in white matter fibre integrity between children with DD and controls using diffusion tensor imaging. White matter integrity and behavioural measures were evaluated in 15 children with developmental dyscalculia aged around 10 years and 15 matched controls. The main finding, obtained by a whole brain group comparison, revealed reduced fractional anisotropy in the superior longitudinal fasciculus in children with developmental dyscalculia. In addition, a region of interest analysis exhibited prominent deficits in fibres of the superior longitudinal fasciculus adjacent to the intraparietal sulcus, which is thought to be the core region for number processing. To conclude, our results outline deficient fibre projection between parietal, temporal and frontal regions in children with developmental dyscalculia, and therefore raise the question of whether dyscalculia can be seen as a dysconnection syndrome. Since the superior longitudinal fasciculus is involved in the integration and control of distributed brain processes, the present results highlight the importance of considering broader domain-general mechanisms in the diagnosis and therapy of dyscalculia.

The "where" and "what" in developmental dyscalculia.

Developmental dyscalculia (DD) is a congenital deficit that affects the ability to acquire arithmetical skills. Individuals with DD have problems learning standard number facts and procedures. Estimates of the prevalence rate of DD are similar to those of developmental dyslexia. Recent reports and discussions suggest that those with DD suffer from specific deficits (e.g., subitizing, comparative judgment). Accordingly, DD has been described as a domain-specific disorder that involves particular brain areas (e.g., intra-parietal sulcus). However, we and others have found that DD is characterized by additional deficiencies and may be affected by domain-general (e.g., attention) factors. Hence "pure DD" might be rather rare and not as pure as one would think. We suggest that the heterogeneity of symptoms that commonly characterize learning disabilities needs to be taken into account in future research and treatment.

Gerstmann meets Geschwind: a crossing (or kissing) variant of a subcortical disconnection syndrome?

That disconnection causes clinical symptoms is a very influential concept in behavioral neurology. Criteria for subcortical disconnection usually are symptoms that are distinct from those following cortical lesions and damage to a single, long-range fiber tract. Yet, a recent study combining functional magnetic resonance imaging and fiber tracking concluded that a focal lesion in left parietal white matter provides the only tenable explanation for pure Gerstmann's syndrome, an enigmatic tetrad of acalculia, agraphia, finger agnosia, and left-right disorientation. Such a lesion would affect not only a single fiber tract but crossing or "kissing" of different fiber tracts and hence disconnect separate cortical networks. As fiber crossing is prominent in the cerebral white matter, the authors propose an extension to the subcortical disconnection framework that opens the door to ascribing a more diversified clinical phenomenology to white matter damage and ensuing disconnection than has been the case so far.