Dyscalculia is a learning disability affecting the acquisition of arithmetical skills in children with normal intelligence and age-appropriate education. Two hypotheses attempt to explain the main cause of dyscalculia. The first hypothesis suggests that a problem with the core mechanisms of perceiving (non-symbolic) quantities is the cause of dyscalculia (core deficit hypothesis), while the alternative hypothesis suggests that dyscalculics have problems only with the processing of numerical symbols (access deficit hypothesis). In the present study, the symbolic and non-symbolic numerosity processing of typically developing children and children with dyscalculia were examined with functional magnetic resonance imaging (fMRI). Control (n=15, mean age: 11.26) and dyscalculia (n=12, mean age: 11.25) groups were determined using a wide-scale screening process. Participants performed a quantity comparison paradigm in the fMRI with two number conditions (dot and symbol comparison) and two difficulty levels (0.5 and 0.7 ratio). The results showed that the bilateral intraparietal sulcus (IPS), left dorsolateral prefrontal cortex (DLPFC) and left fusiform gyrus (so-called “number form area”) were activated for number perception as well as bilateral occipital and supplementary motor areas. The task difficulty engaged bilateral insular cortex, anterior cingulate cortex, IPS and DLPFC activation. The dyscalculia group showed more activation in the left orbitofrontal cortex, left medial prefrontal cortex and right anterior cingulate cortex than the control group. The dyscalculia group showed left hippocampus activation specifically for the symbolic condition. Increased left hippocampal and left-lateralized frontal network activation suggest increased executive and memory-based compensation mechanisms during symbolic processing for dyscalculics. Overall, our findings support the access deficit hypothesis as a neural basis for dyscalculia.

中文翻译：

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患有计算障碍的儿童在符号数字感知过程中表现出海马功能亢进

计算障碍是一种学习障碍，影响智力正常且受过适龄教育的儿童获得算术技能。两种假设试图解释计算障碍的主要原因。第一个假设表明感知（非符号）数量的核心机制的问题是计算障碍的原因（核心赤字假设），而替代假设表明计算障碍仅在处理数字符号方面存在问题（访问赤字假设） ）。在本研究中，典型发育儿童和计算障碍儿童的符号和非符号数字处理通过功能磁共振成像 (fMRI) 进行检查。对照组（n=15，平均年龄：11.26）和计算障碍（n=12，平均年龄：11）。25) 使用大规模筛选过程确定组。参与者在 fMRI 中执行了具有两个数字条件（点和符号比较）和两个难度级别（0.5 和 0.7 比率）的数量比较范式。结果表明，双侧顶内沟（IPS）、左背外侧前额叶皮层（DLPFC）和左梭状回（所谓的“数字形式区”）被激活用于数字感知以及双侧枕叶和辅助运动区域。任务难度涉及双侧岛叶皮层、前扣带回皮层、IPS 和 DLPFC 激活。与对照组相比，计算障碍组的左侧眶额叶皮层、左侧内侧前额叶皮层和右侧前扣带回皮层的激活程度更高。计算障碍组显示左侧海马体激活，专门用于象征性条件。左海马和左侧额叶网络激活的增加表明在计算障碍的符号处理过程中执行和基于记忆的补偿机制增加。总体而言，我们的研究结果支持将通路缺陷假说作为计算障碍的神经基础。