Üstün Sertaç, Ayyıldız Nazife, Kale Emre H, Mançe Çalışır Öykü, Uran Pınar, Öner Özgür, Olkun Sinan, Çiçek Metehan
Department of Physiology, Ankara University School of Medicine, Ankara, Turkey.
Neuroscience and Neurotechnology Center of Excellence, Ankara, Turkey.
Front Hum Neurosci. 2021 Jul 20;15:687476. doi: 10.3389/fnhum.2021.687476. eCollection 2021.
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 ( = 15, mean age: 11.26) and dyscalculia ( = 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.
计算障碍是一种学习障碍,影响智力正常且接受适龄教育的儿童算术技能的习得。有两种假说试图解释计算障碍的主要成因。第一种假说认为,感知(非符号)数量的核心机制存在问题是计算障碍的成因(核心缺陷假说),而另一种假说则认为,患有计算障碍的人仅在数字符号处理方面存在问题(获取缺陷假说)。在本研究中,通过功能磁共振成像(fMRI)检查了发育正常儿童和患有计算障碍儿童的符号和非符号数字处理能力。使用广泛的筛查程序确定了对照组(n = 15,平均年龄:11.26岁)和计算障碍组(n = 12,平均年龄:11.25岁)。参与者在fMRI中执行数量比较范式,有两种数字条件(点和符号比较)和两个难度级别(0.5和0.7比率)。结果表明,双侧顶内沟(IPS)、左侧背外侧前额叶皮层(DLPFC)和左侧梭状回(所谓的“数字形式区域”)以及双侧枕叶和辅助运动区在数字感知时被激活。任务难度引起双侧岛叶皮层、前扣带回皮层、IPS和DLPFC的激活。与对照组相比,计算障碍组在左侧眶额皮层、左侧内侧前额叶皮层和右侧前扣带回皮层表现出更多激活。计算障碍组在符号条件下左侧海马体特异性激活。左侧海马体和左侧额叶网络激活增加表明,计算障碍者在符号处理过程中基于执行和记忆的补偿机制增强。总体而言,我们的研究结果支持获取缺陷假说作为计算障碍的神经基础。